Thrombin potently enhances swelling-sensitive glutamate efflux from cultured astrocytes
High concentrations of thrombin (Thr) have been linked to neuronal damage in cerebral ischemia and traumatic brain injury. In the present study we found that Thr markedly enhanced swelling‐activated efflux of 3H‐glutamate from cultured astrocytes exposed to hyposmotic medium. Thr (0.5–5 U/mL) elicit...
Saved in:
| Published in | Glia Vol. 55; no. 9; pp. 917 - 925 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.07.2007
|
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | High concentrations of thrombin (Thr) have been linked to neuronal damage in cerebral ischemia and traumatic brain injury. In the present study we found that Thr markedly enhanced swelling‐activated efflux of 3H‐glutamate from cultured astrocytes exposed to hyposmotic medium. Thr (0.5–5 U/mL) elicited small 3H‐glutamate efflux under isosmotic conditions and increased the hyposmotic glutamate efflux by 5‐ to 10‐fold, the maximum effect being observed at 15% osmolarity reduction. These Thr effects involve its protease activity and are fully mimicked by SFFLRN, the synthetic peptide activating protease‐activated receptor‐1. Thr potentiation of 3H‐glutamate efflux was largely dependent on a Thr‐elicited increases in cytosolic Ca2+ (Ca2+i) concentration ([Ca2+]i). Preventing Ca2+i rise by treatment with EGTA‐AM or with the phospholipase C blocker U73122 reduced the Thr‐increased glutamate efflux by 68%. The protein kinase C blockers Go6976 or chelerythrine reduced the Thr effect by 19%–22%, while Ca/calmodulin blocker W7 caused a 63% inhibition. In addition to this Ca2+‐sensitive pathway, Thr effect on glutamate efflux also involved activation of phosphoinositide‐3 kinase (PI3K), since it was reduced by the PI3K inhibitor wortmannin (51% inhibition). Treating cells with EGTA‐AM plus wortmannin essentially abolished Thr‐dependent glutamate efflux. Thr‐activated glutamate release was potently inhibited by the blockers of the volume‐sensitive anion permeability pathway, NPPB (IC50 15.8 μM), DCPIB (IC50 4.2 μM). These results suggest that Thr may contribute to the excitotoxic neuronal injury by elevating extracellular glutamate release from glial cells. Therefore, this work may aid in search of neuroprotective strategies for treating cerebral ischemia and brain trauma. © 2007 Wiley‐Liss, Inc. |
|---|---|
| AbstractList | High concentrations of thrombin (Thr) have been linked to neuronal damage in cerebral ischemia and traumatic brain injury. In the present study we found that Thr markedly enhanced swelling‐activated efflux of
3
H
‐glutamate from cultured astrocytes exposed to hyposmotic medium. Thr (0.5–5 U/mL) elicited small
3
H
‐glutamate efflux under isosmotic conditions and increased the hyposmotic glutamate efflux by 5‐ to 10‐fold, the maximum effect being observed at 15% osmolarity reduction. These Thr effects involve its protease activity and are fully mimicked by SFFLRN, the synthetic peptide activating protease‐activated receptor‐1. Thr potentiation of
3
H
‐glutamate efflux was largely dependent on a Thr‐elicited increases in cytosolic Ca
2+
(Ca
2+
i
) concentration ([Ca
2+
]
i
). Preventing Ca
2+
i
rise by treatment with EGTA‐AM or with the phospholipase C blocker U73122 reduced the Thr‐increased glutamate efflux by 68%. The protein kinase C blockers Go6976 or chelerythrine reduced the Thr effect by 19%–22%, while Ca/calmodulin blocker W7 caused a 63% inhibition. In addition to this Ca
2+
‐sensitive pathway, Thr effect on glutamate efflux also involved activation of phosphoinositide‐3 kinase (PI3K), since it was reduced by the PI3K inhibitor wortmannin (51% inhibition). Treating cells with EGTA‐AM plus wortmannin essentially abolished Thr‐dependent glutamate efflux. Thr‐activated glutamate release was potently inhibited by the blockers of the volume‐sensitive anion permeability pathway, NPPB (IC
50
15.8 μM), DCPIB (IC
50
4.2 μM). These results suggest that Thr may contribute to the excitotoxic neuronal injury by elevating extracellular glutamate release from glial cells. Therefore, this work may aid in search of neuroprotective strategies for treating cerebral ischemia and brain trauma. © 2007 Wiley‐Liss, Inc. High concentrations of thrombin (Thr) have been linked to neuronal damage in cerebral ischemia and traumatic brain injury. In the present study we found that Thr markedly enhanced swelling-activated efflux of (3)H-glutamate from cultured astrocytes exposed to hyposmotic medium. Thr (0.5-5 U/mL) elicited small (3)H-glutamate efflux under isosmotic conditions and increased the hyposmotic glutamate efflux by 5- to 10-fold, the maximum effect being observed at 15% osmolarity reduction. These Thr effects involve its protease activity and are fully mimicked by SFFLRN, the synthetic peptide activating protease-activated receptor-1. Thr potentiation of (3)H-glutamate efflux was largely dependent on a Thr-elicited increases in cytosolic Ca(2+) (Ca(2+) (i)) concentration ([Ca(2+)](i)). Preventing Ca(2+) (i) rise by treatment with EGTA-AM or with the phospholipase C blocker U73122 reduced the Thr-increased glutamate efflux by 68%. The protein kinase C blockers Go6976 or chelerythrine reduced the Thr effect by 19%-22%, while Ca/calmodulin blocker W7 caused a 63% inhibition. In addition to this Ca(2+)-sensitive pathway, Thr effect on glutamate efflux also involved activation of phosphoinositide-3 kinase (PI3K), since it was reduced by the PI3K inhibitor wortmannin (51% inhibition). Treating cells with EGTA-AM plus wortmannin essentially abolished Thr-dependent glutamate efflux. Thr-activated glutamate release was potently inhibited by the blockers of the volume-sensitive anion permeability pathway, NPPB (IC(50) 15.8 microM), DCPIB (IC(50) 4.2 microM), and tamoxifen (IC(50) 6.6 microM. These results suggest that Thr may contribute to the excitotoxic neuronal injury by elevating extracellular glutamate release from glial cells. Therefore, this work may aid in search of neuroprotective strategies for treating cerebral ischemia and brain trauma.High concentrations of thrombin (Thr) have been linked to neuronal damage in cerebral ischemia and traumatic brain injury. In the present study we found that Thr markedly enhanced swelling-activated efflux of (3)H-glutamate from cultured astrocytes exposed to hyposmotic medium. Thr (0.5-5 U/mL) elicited small (3)H-glutamate efflux under isosmotic conditions and increased the hyposmotic glutamate efflux by 5- to 10-fold, the maximum effect being observed at 15% osmolarity reduction. These Thr effects involve its protease activity and are fully mimicked by SFFLRN, the synthetic peptide activating protease-activated receptor-1. Thr potentiation of (3)H-glutamate efflux was largely dependent on a Thr-elicited increases in cytosolic Ca(2+) (Ca(2+) (i)) concentration ([Ca(2+)](i)). Preventing Ca(2+) (i) rise by treatment with EGTA-AM or with the phospholipase C blocker U73122 reduced the Thr-increased glutamate efflux by 68%. The protein kinase C blockers Go6976 or chelerythrine reduced the Thr effect by 19%-22%, while Ca/calmodulin blocker W7 caused a 63% inhibition. In addition to this Ca(2+)-sensitive pathway, Thr effect on glutamate efflux also involved activation of phosphoinositide-3 kinase (PI3K), since it was reduced by the PI3K inhibitor wortmannin (51% inhibition). Treating cells with EGTA-AM plus wortmannin essentially abolished Thr-dependent glutamate efflux. Thr-activated glutamate release was potently inhibited by the blockers of the volume-sensitive anion permeability pathway, NPPB (IC(50) 15.8 microM), DCPIB (IC(50) 4.2 microM), and tamoxifen (IC(50) 6.6 microM. These results suggest that Thr may contribute to the excitotoxic neuronal injury by elevating extracellular glutamate release from glial cells. Therefore, this work may aid in search of neuroprotective strategies for treating cerebral ischemia and brain trauma. High concentrations of thrombin (Thr) have been linked to neuronal damage in cerebral ischemia and traumatic brain injury. In the present study we found that Thr markedly enhanced swelling-activated efflux of (3)H-glutamate from cultured astrocytes exposed to hyposmotic medium. Thr (0.5-5 U/mL) elicited small (3)H-glutamate efflux under isosmotic conditions and increased the hyposmotic glutamate efflux by 5- to 10-fold, the maximum effect being observed at 15% osmolarity reduction. These Thr effects involve its protease activity and are fully mimicked by SFFLRN, the synthetic peptide activating protease-activated receptor-1. Thr potentiation of (3)H-glutamate efflux was largely dependent on a Thr-elicited increases in cytosolic Ca(2+) (Ca(2+) (i)) concentration ([Ca(2+)](i)). Preventing Ca(2+) (i) rise by treatment with EGTA-AM or with the phospholipase C blocker U73122 reduced the Thr-increased glutamate efflux by 68%. The protein kinase C blockers Go6976 or chelerythrine reduced the Thr effect by 19%-22%, while Ca/calmodulin blocker W7 caused a 63% inhibition. In addition to this Ca(2+)-sensitive pathway, Thr effect on glutamate efflux also involved activation of phosphoinositide-3 kinase (PI3K), since it was reduced by the PI3K inhibitor wortmannin (51% inhibition). Treating cells with EGTA-AM plus wortmannin essentially abolished Thr-dependent glutamate efflux. Thr-activated glutamate release was potently inhibited by the blockers of the volume-sensitive anion permeability pathway, NPPB (IC(50) 15.8 microM), DCPIB (IC(50) 4.2 microM), and tamoxifen (IC(50) 6.6 microM. These results suggest that Thr may contribute to the excitotoxic neuronal injury by elevating extracellular glutamate release from glial cells. Therefore, this work may aid in search of neuroprotective strategies for treating cerebral ischemia and brain trauma. High concentrations of thrombin (Thr) have been linked to neuronal damage in cerebral ischemia and traumatic brain injury. In the present study we found that Thr markedly enhanced swelling‐activated efflux of 3H‐glutamate from cultured astrocytes exposed to hyposmotic medium. Thr (0.5–5 U/mL) elicited small 3H‐glutamate efflux under isosmotic conditions and increased the hyposmotic glutamate efflux by 5‐ to 10‐fold, the maximum effect being observed at 15% osmolarity reduction. These Thr effects involve its protease activity and are fully mimicked by SFFLRN, the synthetic peptide activating protease‐activated receptor‐1. Thr potentiation of 3H‐glutamate efflux was largely dependent on a Thr‐elicited increases in cytosolic Ca2+ (Ca2+i) concentration ([Ca2+]i). Preventing Ca2+i rise by treatment with EGTA‐AM or with the phospholipase C blocker U73122 reduced the Thr‐increased glutamate efflux by 68%. The protein kinase C blockers Go6976 or chelerythrine reduced the Thr effect by 19%–22%, while Ca/calmodulin blocker W7 caused a 63% inhibition. In addition to this Ca2+‐sensitive pathway, Thr effect on glutamate efflux also involved activation of phosphoinositide‐3 kinase (PI3K), since it was reduced by the PI3K inhibitor wortmannin (51% inhibition). Treating cells with EGTA‐AM plus wortmannin essentially abolished Thr‐dependent glutamate efflux. Thr‐activated glutamate release was potently inhibited by the blockers of the volume‐sensitive anion permeability pathway, NPPB (IC50 15.8 μM), DCPIB (IC50 4.2 μM). These results suggest that Thr may contribute to the excitotoxic neuronal injury by elevating extracellular glutamate release from glial cells. Therefore, this work may aid in search of neuroprotective strategies for treating cerebral ischemia and brain trauma. © 2007 Wiley‐Liss, Inc. High concentrations of thrombin (Thr) have been linked to neuronal damage in cerebral ischemia and traumatic brain injury. In the present study we found that Thr markedly enhanced swelling-activated efflux of 3H-glutamate from cultured astrocytes exposed to hyposmotic medium. Thr (0.5-5 U/mL) elicited small 3H-glutamate efflux under isosmotic conditions and increased the hyposmotic glutamate efflux by 5- to 10-fold, the maximum effect being observed at 15% osmolarity reduction. These Thr effects involve its protease activity and are fully mimicked by SFFLRN, the synthetic peptide activating protease-activated receptor-1. Thr potentiation of 3H-glutamate efflux was largely dependent on a Thr-elicited increases in cytosolic Ca2+ (Ca2+i) concentration ([Ca2+]i). Preventing Ca2+i rise by treatment with EGTA-AM or with the phospholipase C blocker U73122 reduced the Thr-increased glutamate efflux by 68%. The protein kinase C blockers Go6976 or chelerythrine reduced the Thr effect by 19%-22%, while Ca/calmodulin blocker W7 caused a 63% inhibition. In addition to this Ca2+-sensitive pathway, Thr effect on glutamate efflux also involved activation of phosphoinositide-3 kinase (PI3K), since it was reduced by the PI3K inhibitor wortmannin (51% inhibition). Treating cells with EGTA-AM plus wortmannin essentially abolished Thr-dependent glutamate efflux. Thr-activated glutamate release was potently inhibited by the blockers of the volume-sensitive anion permeability pathway, NPPB (IC50 15.8 M), DCPIB (IC50 4.2 M). These results suggest that Thr may contribute to the excitotoxic neuronal injury by elevating extracellular glutamate release from glial cells. Therefore, this work may aid in search of neuroprotective strategies for treating cerebral ischemia and brain trauma. |
| Author | Pasantes-Morales, Herminia Ramos-Mandujano, Gerardo Vázquez-Juárez, Erika Hernández-Benítez, Reyna |
| Author_xml | – sequence: 1 givenname: Gerardo surname: Ramos-Mandujano fullname: Ramos-Mandujano, Gerardo organization: Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México DF, Mexico – sequence: 2 givenname: Erika surname: Vázquez-Juárez fullname: Vázquez-Juárez, Erika organization: Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México DF, Mexico – sequence: 3 givenname: Reyna surname: Hernández-Benítez fullname: Hernández-Benítez, Reyna organization: Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México DF, Mexico – sequence: 4 givenname: Herminia surname: Pasantes-Morales fullname: Pasantes-Morales, Herminia email: hpasante@ifc.unam.mx organization: Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México DF, Mexico |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17437307$$D View this record in MEDLINE/PubMed |
| BookMark | eNqFkU1r3DAQhkVJSTYfl_6A4lMPBacay7asYwjpJrBsCk1JbmIijzdqZXkryU3239fJJjmU0sLAMPA8wzDvPtvxgyfG3gE_Bs6LTytn8bjgFYg3bAZcNTmAqHfYjDeqzKFUsMf2Y_zOOUyD3GV7IEshBZczdn11F4b-1vpsPSTyyW0y8nfoDcUs3pNz1q_ySD7aZH9RtnJjwh4TZdR1bnzIusnOzOjSGKjNMKYwmE2ieMjedugiHT33A_bt89nV6Xm-uJxfnJ4sciNULfK2kl2pSkDRcmEAUNZcmUoJhLKThZCSmxZRKqpEOTFgFGFRqbppiqYRIA7Yh-3edRh-jhST7m00093oaRijlryqaiGb_4IFL0U91QS-fwbH255avQ62x7DRLz-bAL4FTBhiDNRpYxMmO_gU0DoNXD_Goh9j0U-xTMrHP5TXrX-DYQvfW0ebf5B6vrg4eXHyrWNjoodXB8MPXUshK329nOsv6uZrszxf6qX4DcnZrJ4 |
| CitedBy_id | crossref_primary_10_1371_journal_pone_0031756 crossref_primary_10_3390_biom11040562 crossref_primary_10_1111_j_1471_4159_2009_06418_x crossref_primary_10_1016_j_pathophys_2007_09_009 crossref_primary_10_1124_jpet_107_131110 crossref_primary_10_1158_1055_9965_EPI_10_0658 crossref_primary_10_1177_1759091415605115 crossref_primary_10_1002_jnr_23102 crossref_primary_10_1016_j_siny_2021_101224 crossref_primary_10_1007_s12035_021_02639_9 crossref_primary_10_1111_j_1468_1331_2011_03363_x crossref_primary_10_1124_jpet_107_135475 crossref_primary_10_1523_JNEUROSCI_3193_09_2009 crossref_primary_10_3389_fncel_2020_609947 crossref_primary_10_1007_s00424_007_0343_y crossref_primary_10_1089_neu_2016_4464 crossref_primary_10_1186_s12868_018_0481_5 crossref_primary_10_1002_jcp_21406 crossref_primary_10_1146_annurev_pharmtox_011008_145602 crossref_primary_10_1007_s00701_024_06408_0 crossref_primary_10_1111_j_1471_4159_2008_05560_x crossref_primary_10_1016_j_neuron_2008_04_002 crossref_primary_10_1016_j_expneurol_2009_01_023 crossref_primary_10_1186_1756_6606_5_38 crossref_primary_10_1152_ajpcell_00430_2009 crossref_primary_10_1089_neur_2023_0098 crossref_primary_10_3390_ijms232113625 crossref_primary_10_1002_ardp_202400846 crossref_primary_10_3390_ijms17010084 crossref_primary_10_1007_s11064_008_9632_x crossref_primary_10_1111_j_1471_4159_2008_05312_x crossref_primary_10_1007_s11064_014_1300_8 crossref_primary_10_1186_1756_6606_6_4 crossref_primary_10_1016_j_brainresrev_2007_08_002 crossref_primary_10_1038_s41582_020_00447_8 crossref_primary_10_1159_000113742 crossref_primary_10_1111_j_1471_4159_2008_05510_x crossref_primary_10_1111_jnc_14711 crossref_primary_10_1016_j_neuint_2012_02_018 crossref_primary_10_1038_jcbfm_2009_230 crossref_primary_10_1155_2018_6501031 crossref_primary_10_1113_jphysiol_2010_190777 |
| Cites_doi | 10.1007/s00424-004-1322-1 10.1111/j.1471-4159.2005.03499.x 10.1161/01.STR.0000124127.57946.a1 10.1002/glia.10012 10.1074/jbc.271.21.12133 10.1124/jpet.104.072553 10.1046/j.1471-4159.2003.01268.x 10.1083/jcb.200210115 10.1038/35025229 10.1097/01.WCB.0000100062.36077.84 10.1016/j.expneurol.2005.11.017 10.1046/j.1471-4159.2003.02021.x 10.1016/j.expneurol.2004.02.018 10.1159/000045829 10.1152/ajpcell.00330.2004 10.1073/pnas.2235594100 10.5483/BMBRep.2002.35.1.067 10.4049/jimmunol.170.5.2638 10.1002/glia.10271 10.1073/pnas.040552897 10.1242/jeb.198.2.311 10.1006/bbrc.1997.6222 10.1016/j.neuint.2005.12.001 10.1523/JNEUROSCI.20-12-04582.2000 10.1016/0304-3940(92)90065-F 10.1016/j.neuroscience.2006.09.049 10.1113/jphysiol.2005.103820 10.1124/jpet.105.098467 10.1038/sj.bjp.0704413 10.1002/glia.20174 10.1046/j.1471-4159.1996.66041374.x 10.1124/jpet.105.090787 10.1046/j.0953-816x.2001.01676.x |
| ContentType | Journal Article |
| Copyright | Copyright © 2007 Wiley‐Liss, Inc. (c) 2007 Wiley-Liss, Inc. |
| Copyright_xml | – notice: Copyright © 2007 Wiley‐Liss, Inc. – notice: (c) 2007 Wiley-Liss, Inc. |
| DBID | BSCLL AAYXX CITATION CGR CUY CVF ECM EIF NPM 7QP 7TK 7X8 |
| DOI | 10.1002/glia.20513 |
| DatabaseName | Istex CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Calcium & Calcified Tissue Abstracts Neurosciences Abstracts MEDLINE - Academic |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Calcium & Calcified Tissue Abstracts Neurosciences Abstracts MEDLINE - Academic |
| DatabaseTitleList | CrossRef MEDLINE - Academic MEDLINE Calcium & Calcified Tissue Abstracts |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Anatomy & Physiology |
| EISSN | 1098-1136 |
| EndPage | 925 |
| ExternalDocumentID | 17437307 10_1002_glia_20513 GLIA20513 ark_67375_WNG_P9XS8NHN_N |
| Genre | article Journal Article |
| GrantInformation_xml | – fundername: DGAPA, UNAM funderid: 209507 – fundername: CONACYT, México funderid: 46465 |
| GroupedDBID | --- -~X .3N .55 .GA .GJ .Y3 05W 0R~ 10A 1L6 1OB 1OC 1ZS 31~ 33P 3SF 3WU 4.4 4ZD 50Y 50Z 51W 51X 52M 52N 52O 52P 52S 52T 52U 52W 52X 53G 5GY 5RE 5VS 66C 702 7PT 8-0 8-1 8-3 8-4 8-5 8UM 930 A03 AAESR AAEVG AAHHS AANLZ AAONW AASGY AAXRX AAZKR ABCQN ABCUV ABEML ABIJN ABIVO ABJNI ABPVW ACAHQ ACBWZ ACCFJ ACCZN ACGFS ACPOU ACPRK ACSCC ACXBN ACXQS ADBBV ADEOM ADIZJ ADKYN ADMGS ADOZA ADXAS ADZMN ADZOD AEEZP AEIGN AEIMD AENEX AEQDE AEUQT AEUYR AFBPY AFFNX AFFPM AFGKR AFPWT AFRAH AFZJQ AHBTC AHMBA AITYG AIURR AIWBW AJBDE AJXKR ALAGY ALMA_UNASSIGNED_HOLDINGS ALUQN AMBMR AMYDB ASPBG ATUGU AUFTA AVWKF AZBYB AZFZN AZVAB BAFTC BDRZF BFHJK BHBCM BMNLL BMXJE BNHUX BROTX BRXPI BSCLL BY8 C45 CS3 D-E D-F DCZOG DPXWK DR1 DR2 DRFUL DRSTM DU5 EBD EBS EJD EMOBN F00 F01 F04 F5P FEDTE G-S G.N GAKWD GNP GODZA H.T H.X HBH HF~ HGLYW HHY HHZ HVGLF HZ~ IX1 J0M JPC KQQ LATKE LAW LC2 LC3 LEEKS LH4 LITHE LOXES LP6 LP7 LUTES LW6 LYRES M6M MEWTI MK4 MRFUL MRSTM MSFUL MSSTM MXFUL MXSTM N04 N05 N9A NF~ NNB O66 O9- OIG OVD P2P P2W P2X P4D PALCI PQQKQ Q.N Q11 QB0 QRW R.K RIWAO RJQFR ROL RWD RWI RX1 RYL SAMSI SUPJJ SV3 TEORI UB1 V2E W8V W99 WBKPD WIB WIH WIK WJL WNSPC WOHZO WQJ WRC WUP WXSBR WYISQ X7M XG1 XV2 ZGI ZXP ZZTAW ~IA ~WT AAHQN AAMNL AANHP AAYCA ACRPL ACYXJ ADNMO AFWVQ ALVPJ AAYXX AEYWJ AGHNM AGQPQ AGYGG CITATION CGR CUY CVF ECM EIF NPM 7QP 7TK AAMMB AEFGJ AGXDD AIDQK AIDYY 7X8 |
| ID | FETCH-LOGICAL-c3963-d57f4941a3d03c11a7609c593a14f723770cdaa79e5343d01c9ea259688288313 |
| IEDL.DBID | DR2 |
| ISSN | 0894-1491 |
| IngestDate | Thu Jul 10 22:57:58 EDT 2025 Fri Jul 11 11:19:12 EDT 2025 Wed Feb 19 01:43:21 EST 2025 Tue Jul 01 02:14:55 EDT 2025 Thu Apr 24 23:06:49 EDT 2025 Wed Jan 22 16:15:31 EST 2025 Wed Oct 30 09:56:19 EDT 2024 |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 9 |
| Language | English |
| License | http://onlinelibrary.wiley.com/termsAndConditions#vor (c) 2007 Wiley-Liss, Inc. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c3963-d57f4941a3d03c11a7609c593a14f723770cdaa79e5343d01c9ea259688288313 |
| Notes | ArticleID:GLIA20513 istex:9F3F46B81CC55981C59D783570828A0481246484 CONACYT, México - No. 46465 ark:/67375/WNG-P9XS8NHN-N DGAPA, UNAM - No. 209507 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| PMID | 17437307 |
| PQID | 20436436 |
| PQPubID | 23462 |
| PageCount | 9 |
| ParticipantIDs | proquest_miscellaneous_70556378 proquest_miscellaneous_20436436 pubmed_primary_17437307 crossref_citationtrail_10_1002_glia_20513 crossref_primary_10_1002_glia_20513 wiley_primary_10_1002_glia_20513_GLIA20513 istex_primary_ark_67375_WNG_P9XS8NHN_N |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2007-07 July 2007 2007-07-00 2007-Jul 20070701 |
| PublicationDateYYYYMMDD | 2007-07-01 |
| PublicationDate_xml | – month: 07 year: 2007 text: 2007-07 |
| PublicationDecade | 2000 |
| PublicationPlace | Hoboken |
| PublicationPlace_xml | – name: Hoboken – name: United States |
| PublicationTitle | Glia |
| PublicationTitleAlternate | Glia |
| PublicationYear | 2007 |
| Publisher | Wiley Subscription Services, Inc., A Wiley Company |
| Publisher_xml | – name: Wiley Subscription Services, Inc., A Wiley Company |
| References | Abdullaev IF,Rudkouskaya A,Schools GP,Kimelberg HK,Mongin AA. 2006. Pharmacological comparison of swelling-activated excitatory amino acid release and Cl- currents in cultured rat astrocytes. J Physiol 572: 677-689. Heacock AM,Dodd MS,Fisher SK. 2006. Regulation of volume-sensitive osmolyte efflux from human SH-SY5Y neuroblastoma cells following activation of lysophospholipid receptors. J Pharmacol Exp Ther 317: 685-693. Decher N,Lang HJ,Nilius B,Bruggemann A,Busch AE,Steinmeyer K. 2001. DCPIB is a novel selective blocker of I(Cl,swell) and prevents swelling-induced shortening of guinea-pig atrial action potential duration. Br J Pharmacol 134; 1467-1479. Kawai H,Yuki S,Sugimoto J,Tamao Y. 1996. Effects of a thrombin inhibitor, argatroban, on ischemic brain damage in the rat distal middle cerebral artery occlusion model. J Pharmacol Exp Ther 278: 780-785. Junge CE,Lee CJ,Hubbard KB,Zhang Z,Olson JJ,Hepler JR,Brat DJ,Traynelis SF. 2004. Protease-activated receptor-1 in human brain: Localization and functional expression in astrocytes. Exp Neurol 188: 94-103. Cheema TA,Ward CE,Fisher SK. 2005. Subnanomolar concentrations of thrombin enhance the volume-sensitive efflux of taurine from human 1321N1 astrocytoma cells. J Pharmacol Exp Ther 315: 755-763. Pasantes-Morales H,Morales Mulia S. 2000. Influence of calcium on regulatory volume decrease: Role of potassium channels. Nephron 86: 414-427. Weinstein JR,Hong S,Kulman JD,Bishop C,Kuniyoshi J,Andersen H,Ransom BR,Hanisch UK,Moller T. 2005. Unraveling thrombin's true microglia-activating potential: Markedly disparate profiles of pharmaceutical-grade and commercial-grade thrombin preparations. J Neurochem 95: 1177-1187. Mongin AA,Kimelberg HK. 2005. ATP regulates anion channel-mediated organic osmolyte release from cultured rat astrocytes via multiple Ca2+-sensitive mechanisms. Am J Physiol Cell Physiol 288: C204-C213. Yi JH,Hazell AS. 2006. Excitotoxic mechanisms and the role of astrocytic glutamate transporters in traumatic brain injury. Neurochem Int 48: 394-403. Coughlin SR. 2000. Thrombin signalling and protease-activated receptors. Nature 407: 258-264. Pike CJ,Vaughan PJ,Cunningham DD,Connan CW. 1996. Thrombin attenuates neuronal cell death and modulates astrocyte reactivity induced by β-amyloid in vitro. J Neurochem 66: 1374-1382. Feustel PJ,Jin Y,Kimelberg HK. 2004. Volume-regulated anion channels are the predominant contributors to release of excitatory amino acids in the ischemic cortical penumbra. Stroke 35: 1164-1168. Gingrich MB,Junge CE,Lyuboslavsky P,Traynelis SF. 2000. Potentiation of NMDA receptor function by the serine protease thrombin. J Neurosci 20: 4582-4595. Striggow F,Riek-Burchardt M,Kiesel A,Schmidt W,Henrich-Noack P,Breder J,Krug M,Reymann KG,Reiser G. 2001. Four different types of protease-activated receptors are widely expressed in the brain and are up regulated in hippocampus by severe ischemia. Eur J Neurosci 14: 595-608. Loveday D,Heacock AM,Fisher SK. 2003. Activation of muscarinic cholinergic receptors enhances the volume-sensitive efflux of myo-inositol from SH-SY5Y neuroblastoma cells. J Neurochem. 87: 476-486. Xi G,Hua Y,Wu J,Keep RF. 2002. Increase of brain thrombin concentration in cerebral ischemia. Stroke 33: 399 Karabiyikoglu M,Hua Y,Keep RF,Ennis SR,Xi G. 2004. Intracerebral hirudin injection attenuates ischemic damage and neurologic deficits without altering local cerebral blood flow. J Cereb Blood Flow Metab 24: 159-166. Cardin V,Lezama R,Torres-Marquez ME,Pasantes-Morales H. 2003. Potentiation of the osmosensitive taurine release and cell volume regulation by Ca2+i rise in cultured cerebellar astrocytes. Glia 44: 119-128. Kimelberg HK. 2005. Astrocytic swelling in cerebral ischemia as a possible cause of injury and target for therapy. Glia 50: 389-397. Fujimoto S,Katsuki H,Ohnishi M,Takagi M,Kume T,Akaike A. 2007. Thrombin induces striatal neurotoxicity depending on mitogen-activated protein kinase pathways in vivo. Neuroscience 144: 694-701. Won SJ,Kim DY,Gwag BJ. 2002. Cellular and molecular pathways of ischemic neuronal death. J Biochem Mol Biol 35: 67-86. Boven LA,Vergnolle N,Henry SD,Silva C,Imai Y,Holden J,Warren K,Hollenberg MD,Power C. 2003. Up-regulation of proteinase-activated receptor 1 expression in astrocytes during HIV encephalitis. J Immunol 170: 2638-2646. Akiyama H,Ikeda K,Kondo H,McGeer PL. 1992. Thrombin accumulation in brains of patients with Alzheimer's disease. Neurosci Lett 146: 152-154. Junge CE,Sugawara T,Mannaioni G,Alagarsamy S,Conn PJ,Brat DJ,Chan PH,Traynelis SF. 2003. The contribution of protease-activated receptor 1 to neuronal damage caused by transient focal cerebral ischemia. Proc Natl Acad Sci USA 100: 13019-13024. De Castro Ribeiro M,Badaut J,Price M,Meins M,Bogousslavsky J,Monard D,Hirt L. 2006. Thrombin in ischemic neuronal death. Exp Neurol 198: 199-203. Hawes BE,Luttrell LM,van Biesen T,Lefkowitz RJ. 1996. Phosphatidylinositol 3-kinase is an early intermediate in the Gβγ-mediated mitogen-activated protein kinase signaling pathway. J Biol Chem 271: 12133-12136. BrocK C,Schaefer M,Reusch HP,Chupalla C,Michalke M,Spicher K,Schultz G,Nurberg B. 2003. Roles of G β γ in membrane recruitment and activation of p110/p101 phosphoinositide 3-kinase γ. J Cell Biol 160: 89-99. Thoroed S,Soergaard M,Cragoe E,Fugelli K. 1995. The osmolality-sensitive taurine channel in flounder erythrocytes is strongly stimulated by noradrenaline under hypo-osmotic conditions. J Exp Biol 198: 311-324. Wang H,Ubl JJ,Reiser G. 2002. Four subtypes of protease-activated receptors, co-expressed in rat astrocytes, evoke different physiological signaling. Glia 37: 53-63. Xi G,Reiser G,Keep RF. 2003. The role of thrombin and thrombin receptors in ischemic, hemorrhagic and traumatic brain injury: Deleterious or protective? J Neurochem 84: 3-9. Franco R,Rodríguez R,Pasantes-Morales H. 2004. Mechanisms of the ATP potentiation of hyposmotic taurine release in Swiss 3T3 fibroblasts. Pflugers Arch Eur J Physiol 449: 159-169. Heacock AM,Kerley D,Gurda GT,VanTroostenberghe AT,Fisher SK. 2004. Potentiation of the osmosensitive release of taurine and D-aspartate from SH-SY5Y neuroblastoma cells after activation of M3 muscarinic cholinergic receptors. J Pharmacol Exp Ther 311: 1097-1104. Striggow F,Riek M,Breder J,Henrich-Noack P,Reymann KG,Reiser G. 2000. The protease thrombin is an endogenous mediator of hippocampal neuroprotection against ischemia at low concentrations but causes degeneration at high concentrations. Proc Natl Acad Sci USA 97: 2264-2269. Manolopoulos VG,Droogmans G,Nilius B. 1997. Hypotonicity and thrombin activate taurine efflux in BC3H1 and C2C12 myoblasts that is down regulated during differentiation. Biochem Biophys Res Commun 232: 74-79. 2004; 188 2002; 37 2006; 317 1992; 146 2007; 144 2002; 35 1997; 232 2005; 315 2000; 20 2004; 24 2000; 86 2002; 33 2006; 572 2006; 198 2003; 170 2004; 449 1995; 198 2000; 407 2001; 134 2004; 311 2005; 288 2004; 35 2000; 97 2006; 48 2005; 95 1996; 271 2003; 160 2005; 50 1996; 278 2003; 84 2001; 14 2003; 100 2003; 87 2003; 44 1996; 66 e_1_2_6_32_1 Xi G (e_1_2_6_34_1) 2002; 33 e_1_2_6_10_1 e_1_2_6_31_1 e_1_2_6_19_1 e_1_2_6_13_1 e_1_2_6_36_1 e_1_2_6_35_1 e_1_2_6_11_1 e_1_2_6_12_1 e_1_2_6_33_1 e_1_2_6_17_1 e_1_2_6_18_1 e_1_2_6_15_1 e_1_2_6_16_1 Thoroed S (e_1_2_6_30_1) 1995; 198 e_1_2_6_20_1 e_1_2_6_9_1 e_1_2_6_8_1 e_1_2_6_5_1 e_1_2_6_4_1 e_1_2_6_7_1 e_1_2_6_6_1 Kawai H (e_1_2_6_21_1) 1996; 278 e_1_2_6_25_1 Gingrich MB (e_1_2_6_14_1) 2000; 20 e_1_2_6_24_1 e_1_2_6_3_1 e_1_2_6_23_1 e_1_2_6_2_1 e_1_2_6_22_1 e_1_2_6_29_1 e_1_2_6_28_1 e_1_2_6_27_1 e_1_2_6_26_1 |
| References_xml | – reference: Xi G,Hua Y,Wu J,Keep RF. 2002. Increase of brain thrombin concentration in cerebral ischemia. Stroke 33: 399 – reference: Cheema TA,Ward CE,Fisher SK. 2005. Subnanomolar concentrations of thrombin enhance the volume-sensitive efflux of taurine from human 1321N1 astrocytoma cells. J Pharmacol Exp Ther 315: 755-763. – reference: Abdullaev IF,Rudkouskaya A,Schools GP,Kimelberg HK,Mongin AA. 2006. Pharmacological comparison of swelling-activated excitatory amino acid release and Cl- currents in cultured rat astrocytes. J Physiol 572: 677-689. – reference: Karabiyikoglu M,Hua Y,Keep RF,Ennis SR,Xi G. 2004. Intracerebral hirudin injection attenuates ischemic damage and neurologic deficits without altering local cerebral blood flow. J Cereb Blood Flow Metab 24: 159-166. – reference: Thoroed S,Soergaard M,Cragoe E,Fugelli K. 1995. The osmolality-sensitive taurine channel in flounder erythrocytes is strongly stimulated by noradrenaline under hypo-osmotic conditions. J Exp Biol 198: 311-324. – reference: Striggow F,Riek-Burchardt M,Kiesel A,Schmidt W,Henrich-Noack P,Breder J,Krug M,Reymann KG,Reiser G. 2001. Four different types of protease-activated receptors are widely expressed in the brain and are up regulated in hippocampus by severe ischemia. Eur J Neurosci 14: 595-608. – reference: Weinstein JR,Hong S,Kulman JD,Bishop C,Kuniyoshi J,Andersen H,Ransom BR,Hanisch UK,Moller T. 2005. Unraveling thrombin's true microglia-activating potential: Markedly disparate profiles of pharmaceutical-grade and commercial-grade thrombin preparations. J Neurochem 95: 1177-1187. – reference: Akiyama H,Ikeda K,Kondo H,McGeer PL. 1992. Thrombin accumulation in brains of patients with Alzheimer's disease. Neurosci Lett 146: 152-154. – reference: Decher N,Lang HJ,Nilius B,Bruggemann A,Busch AE,Steinmeyer K. 2001. DCPIB is a novel selective blocker of I(Cl,swell) and prevents swelling-induced shortening of guinea-pig atrial action potential duration. Br J Pharmacol 134; 1467-1479. – reference: Pike CJ,Vaughan PJ,Cunningham DD,Connan CW. 1996. Thrombin attenuates neuronal cell death and modulates astrocyte reactivity induced by β-amyloid in vitro. J Neurochem 66: 1374-1382. – reference: Cardin V,Lezama R,Torres-Marquez ME,Pasantes-Morales H. 2003. Potentiation of the osmosensitive taurine release and cell volume regulation by Ca2+i rise in cultured cerebellar astrocytes. Glia 44: 119-128. – reference: Heacock AM,Kerley D,Gurda GT,VanTroostenberghe AT,Fisher SK. 2004. Potentiation of the osmosensitive release of taurine and D-aspartate from SH-SY5Y neuroblastoma cells after activation of M3 muscarinic cholinergic receptors. J Pharmacol Exp Ther 311: 1097-1104. – reference: Feustel PJ,Jin Y,Kimelberg HK. 2004. Volume-regulated anion channels are the predominant contributors to release of excitatory amino acids in the ischemic cortical penumbra. Stroke 35: 1164-1168. – reference: Junge CE,Sugawara T,Mannaioni G,Alagarsamy S,Conn PJ,Brat DJ,Chan PH,Traynelis SF. 2003. The contribution of protease-activated receptor 1 to neuronal damage caused by transient focal cerebral ischemia. Proc Natl Acad Sci USA 100: 13019-13024. – reference: Striggow F,Riek M,Breder J,Henrich-Noack P,Reymann KG,Reiser G. 2000. The protease thrombin is an endogenous mediator of hippocampal neuroprotection against ischemia at low concentrations but causes degeneration at high concentrations. Proc Natl Acad Sci USA 97: 2264-2269. – reference: Gingrich MB,Junge CE,Lyuboslavsky P,Traynelis SF. 2000. Potentiation of NMDA receptor function by the serine protease thrombin. J Neurosci 20: 4582-4595. – reference: Kimelberg HK. 2005. Astrocytic swelling in cerebral ischemia as a possible cause of injury and target for therapy. Glia 50: 389-397. – reference: Boven LA,Vergnolle N,Henry SD,Silva C,Imai Y,Holden J,Warren K,Hollenberg MD,Power C. 2003. Up-regulation of proteinase-activated receptor 1 expression in astrocytes during HIV encephalitis. J Immunol 170: 2638-2646. – reference: Coughlin SR. 2000. Thrombin signalling and protease-activated receptors. Nature 407: 258-264. – reference: Franco R,Rodríguez R,Pasantes-Morales H. 2004. Mechanisms of the ATP potentiation of hyposmotic taurine release in Swiss 3T3 fibroblasts. Pflugers Arch Eur J Physiol 449: 159-169. – reference: Junge CE,Lee CJ,Hubbard KB,Zhang Z,Olson JJ,Hepler JR,Brat DJ,Traynelis SF. 2004. Protease-activated receptor-1 in human brain: Localization and functional expression in astrocytes. Exp Neurol 188: 94-103. – reference: De Castro Ribeiro M,Badaut J,Price M,Meins M,Bogousslavsky J,Monard D,Hirt L. 2006. Thrombin in ischemic neuronal death. Exp Neurol 198: 199-203. – reference: Wang H,Ubl JJ,Reiser G. 2002. Four subtypes of protease-activated receptors, co-expressed in rat astrocytes, evoke different physiological signaling. Glia 37: 53-63. – reference: Xi G,Reiser G,Keep RF. 2003. The role of thrombin and thrombin receptors in ischemic, hemorrhagic and traumatic brain injury: Deleterious or protective? J Neurochem 84: 3-9. – reference: Yi JH,Hazell AS. 2006. Excitotoxic mechanisms and the role of astrocytic glutamate transporters in traumatic brain injury. Neurochem Int 48: 394-403. – reference: Heacock AM,Dodd MS,Fisher SK. 2006. Regulation of volume-sensitive osmolyte efflux from human SH-SY5Y neuroblastoma cells following activation of lysophospholipid receptors. J Pharmacol Exp Ther 317: 685-693. – reference: Won SJ,Kim DY,Gwag BJ. 2002. Cellular and molecular pathways of ischemic neuronal death. J Biochem Mol Biol 35: 67-86. – reference: Fujimoto S,Katsuki H,Ohnishi M,Takagi M,Kume T,Akaike A. 2007. Thrombin induces striatal neurotoxicity depending on mitogen-activated protein kinase pathways in vivo. Neuroscience 144: 694-701. – reference: Mongin AA,Kimelberg HK. 2005. ATP regulates anion channel-mediated organic osmolyte release from cultured rat astrocytes via multiple Ca2+-sensitive mechanisms. Am J Physiol Cell Physiol 288: C204-C213. – reference: BrocK C,Schaefer M,Reusch HP,Chupalla C,Michalke M,Spicher K,Schultz G,Nurberg B. 2003. Roles of G β γ in membrane recruitment and activation of p110/p101 phosphoinositide 3-kinase γ. J Cell Biol 160: 89-99. – reference: Manolopoulos VG,Droogmans G,Nilius B. 1997. Hypotonicity and thrombin activate taurine efflux in BC3H1 and C2C12 myoblasts that is down regulated during differentiation. Biochem Biophys Res Commun 232: 74-79. – reference: Loveday D,Heacock AM,Fisher SK. 2003. Activation of muscarinic cholinergic receptors enhances the volume-sensitive efflux of myo-inositol from SH-SY5Y neuroblastoma cells. J Neurochem. 87: 476-486. – reference: Pasantes-Morales H,Morales Mulia S. 2000. Influence of calcium on regulatory volume decrease: Role of potassium channels. Nephron 86: 414-427. – reference: Kawai H,Yuki S,Sugimoto J,Tamao Y. 1996. Effects of a thrombin inhibitor, argatroban, on ischemic brain damage in the rat distal middle cerebral artery occlusion model. J Pharmacol Exp Ther 278: 780-785. – reference: Hawes BE,Luttrell LM,van Biesen T,Lefkowitz RJ. 1996. Phosphatidylinositol 3-kinase is an early intermediate in the Gβγ-mediated mitogen-activated protein kinase signaling pathway. J Biol Chem 271: 12133-12136. – volume: 134 start-page: 1467 year: 2001 end-page: 1479 article-title: DCPIB is a novel selective blocker of I(Cl,swell) and prevents swelling‐induced shortening of guinea‐pig atrial action potential duration publication-title: Br J Pharmacol – volume: 50 start-page: 389 year: 2005 end-page: 397 article-title: Astrocytic swelling in cerebral ischemia as a possible cause of injury and target for therapy publication-title: Glia – volume: 288 start-page: C204 year: 2005 end-page: C213 article-title: ATP regulates anion channel‐mediated organic osmolyte release from cultured rat astrocytes via multiple Ca ‐sensitive mechanisms publication-title: Am J Physiol Cell Physiol – volume: 315 start-page: 755 year: 2005 end-page: 763 article-title: Subnanomolar concentrations of thrombin enhance the volume‐sensitive efflux of taurine from human 1321N1 astrocytoma cells publication-title: J Pharmacol Exp Ther – volume: 311 start-page: 1097 year: 2004 end-page: 1104 article-title: Potentiation of the osmosensitive release of taurine and ‐aspartate from SH‐SY5Y neuroblastoma cells after activation of M3 muscarinic cholinergic receptors publication-title: J Pharmacol Exp Ther – volume: 100 start-page: 13019 year: 2003 end-page: 13024 article-title: The contribution of protease‐activated receptor 1 to neuronal damage caused by transient focal cerebral ischemia publication-title: Proc Natl Acad Sci USA – volume: 35 start-page: 1164 year: 2004 end-page: 1168 article-title: Volume‐regulated anion channels are the predominant contributors to release of excitatory amino acids in the ischemic cortical penumbra publication-title: Stroke – volume: 278 start-page: 780 year: 1996 end-page: 785 article-title: Effects of a thrombin inhibitor, argatroban, on ischemic brain damage in the rat distal middle cerebral artery occlusion model publication-title: J Pharmacol Exp Ther – volume: 44 start-page: 119 year: 2003 end-page: 128 article-title: Potentiation of the osmosensitive taurine release and cell volume regulation by Ca rise in cultured cerebellar astrocytes publication-title: Glia – volume: 48 start-page: 394 year: 2006 end-page: 403 article-title: Excitotoxic mechanisms and the role of astrocytic glutamate transporters in traumatic brain injury publication-title: Neurochem Int – volume: 407 start-page: 258 year: 2000 end-page: 264 article-title: Thrombin signalling and protease‐activated receptors publication-title: Nature – volume: 14 start-page: 595 year: 2001 end-page: 608 article-title: Four different types of protease‐activated receptors are widely expressed in the brain and are up regulated in hippocampus by severe ischemia publication-title: Eur J Neurosci – volume: 20 start-page: 4582 year: 2000 end-page: 4595 article-title: Potentiation of NMDA receptor function by the serine protease thrombin publication-title: J Neurosci – volume: 37 start-page: 53 year: 2002 end-page: 63 article-title: Four subtypes of protease‐activated receptors, co‐expressed in rat astrocytes, evoke different physiological signaling publication-title: Glia – volume: 97 start-page: 2264 year: 2000 end-page: 2269 article-title: The protease thrombin is an endogenous mediator of hippocampal neuroprotection against ischemia at low concentrations but causes degeneration at high concentrations publication-title: Proc Natl Acad Sci USA – volume: 198 start-page: 311 year: 1995 end-page: 324 article-title: The osmolality‐sensitive taurine channel in flounder erythrocytes is strongly stimulated by noradrenaline under hypo‐osmotic conditions publication-title: J Exp Biol – volume: 317 start-page: 685 year: 2006 end-page: 693 article-title: Regulation of volume‐sensitive osmolyte efflux from human SH‐SY5Y neuroblastoma cells following activation of lysophospholipid receptors publication-title: J Pharmacol Exp Ther – volume: 84 start-page: 3 year: 2003 end-page: 9 article-title: The role of thrombin and thrombin receptors in ischemic, hemorrhagic and traumatic brain injury: Deleterious or protective? publication-title: J Neurochem – volume: 35 start-page: 67 year: 2002 end-page: 86 article-title: Cellular and molecular pathways of ischemic neuronal death publication-title: J Biochem Mol Biol – volume: 188 start-page: 94 year: 2004 end-page: 103 article-title: Protease‐activated receptor‐1 in human brain: Localization and functional expression in astrocytes publication-title: Exp Neurol – volume: 449 start-page: 159 year: 2004 end-page: 169 article-title: Mechanisms of the ATP potentiation of hyposmotic taurine release in Swiss 3T3 fibroblasts publication-title: Pflugers Arch Eur J Physiol – volume: 572 start-page: 677 year: 2006 end-page: 689 article-title: Pharmacological comparison of swelling‐activated excitatory amino acid release and Cl‐ currents in cultured rat astrocytes publication-title: J Physiol – volume: 24 start-page: 159 year: 2004 end-page: 166 article-title: Intracerebral hirudin injection attenuates ischemic damage and neurologic deficits without altering local cerebral blood flow publication-title: J Cereb Blood Flow Metab – volume: 271 start-page: 12133 year: 1996 end-page: 12136 article-title: Phosphatidylinositol 3‐kinase is an early intermediate in the Gβγ‐mediated mitogen‐activated protein kinase signaling pathway publication-title: J Biol Chem – volume: 95 start-page: 1177 year: 2005 end-page: 1187 article-title: Unraveling thrombin's true microglia‐activating potential: Markedly disparate profiles of pharmaceutical‐grade and commercial‐grade thrombin preparations publication-title: J Neurochem – volume: 66 start-page: 1374 year: 1996 end-page: 1382 article-title: Thrombin attenuates neuronal cell death and modulates astrocyte reactivity induced by β‐amyloid in vitro publication-title: J Neurochem – volume: 86 start-page: 414 year: 2000 end-page: 427 article-title: Influence of calcium on regulatory volume decrease: Role of potassium channels publication-title: Nephron – volume: 144 start-page: 694 year: 2007 end-page: 701 article-title: Thrombin induces striatal neurotoxicity depending on mitogen‐activated protein kinase pathways in vivo publication-title: Neuroscience – volume: 87 start-page: 476 year: 2003 end-page: 486 article-title: Activation of muscarinic cholinergic receptors enhances the volume‐sensitive efflux of myo‐inositol from SH‐SY5Y neuroblastoma cells publication-title: J Neurochem. – volume: 170 start-page: 2638 year: 2003 end-page: 2646 article-title: Up‐regulation of proteinase‐activated receptor 1 expression in astrocytes during HIV encephalitis publication-title: J Immunol – volume: 146 start-page: 152 year: 1992 end-page: 154 article-title: Thrombin accumulation in brains of patients with Alzheimer's disease publication-title: Neurosci Lett – volume: 160 start-page: 89 year: 2003 end-page: 99 article-title: Roles of G β γ in membrane recruitment and activation of p110/p101 phosphoinositide 3‐kinase γ publication-title: J Cell Biol – volume: 33 start-page: 399 year: 2002 article-title: Increase of brain thrombin concentration in cerebral ischemia publication-title: Stroke – volume: 198 start-page: 199 year: 2006 end-page: 203 article-title: Thrombin in ischemic neuronal death publication-title: Exp Neurol – volume: 232 start-page: 74 year: 1997 end-page: 79 article-title: Hypotonicity and thrombin activate taurine efflux in BC3H1 and C2C12 myoblasts that is down regulated during differentiation publication-title: Biochem Biophys Res Commun – ident: e_1_2_6_12_1 doi: 10.1007/s00424-004-1322-1 – ident: e_1_2_6_32_1 doi: 10.1111/j.1471-4159.2005.03499.x – ident: e_1_2_6_11_1 doi: 10.1161/01.STR.0000124127.57946.a1 – ident: e_1_2_6_31_1 doi: 10.1002/glia.10012 – ident: e_1_2_6_15_1 doi: 10.1074/jbc.271.21.12133 – volume: 33 start-page: 399 year: 2002 ident: e_1_2_6_34_1 article-title: Increase of brain thrombin concentration in cerebral ischemia publication-title: Stroke – ident: e_1_2_6_17_1 doi: 10.1124/jpet.104.072553 – ident: e_1_2_6_35_1 doi: 10.1046/j.1471-4159.2003.01268.x – ident: e_1_2_6_5_1 doi: 10.1083/jcb.200210115 – ident: e_1_2_6_8_1 doi: 10.1038/35025229 – ident: e_1_2_6_20_1 doi: 10.1097/01.WCB.0000100062.36077.84 – ident: e_1_2_6_9_1 doi: 10.1016/j.expneurol.2005.11.017 – ident: e_1_2_6_23_1 doi: 10.1046/j.1471-4159.2003.02021.x – ident: e_1_2_6_18_1 doi: 10.1016/j.expneurol.2004.02.018 – ident: e_1_2_6_26_1 doi: 10.1159/000045829 – ident: e_1_2_6_25_1 doi: 10.1152/ajpcell.00330.2004 – ident: e_1_2_6_19_1 doi: 10.1073/pnas.2235594100 – ident: e_1_2_6_33_1 doi: 10.5483/BMBRep.2002.35.1.067 – ident: e_1_2_6_4_1 doi: 10.4049/jimmunol.170.5.2638 – ident: e_1_2_6_6_1 doi: 10.1002/glia.10271 – ident: e_1_2_6_28_1 doi: 10.1073/pnas.040552897 – volume: 278 start-page: 780 year: 1996 ident: e_1_2_6_21_1 article-title: Effects of a thrombin inhibitor, argatroban, on ischemic brain damage in the rat distal middle cerebral artery occlusion model publication-title: J Pharmacol Exp Ther – volume: 198 start-page: 311 year: 1995 ident: e_1_2_6_30_1 article-title: The osmolality‐sensitive taurine channel in flounder erythrocytes is strongly stimulated by noradrenaline under hypo‐osmotic conditions publication-title: J Exp Biol doi: 10.1242/jeb.198.2.311 – ident: e_1_2_6_24_1 doi: 10.1006/bbrc.1997.6222 – ident: e_1_2_6_36_1 doi: 10.1016/j.neuint.2005.12.001 – volume: 20 start-page: 4582 year: 2000 ident: e_1_2_6_14_1 article-title: Potentiation of NMDA receptor function by the serine protease thrombin publication-title: J Neurosci doi: 10.1523/JNEUROSCI.20-12-04582.2000 – ident: e_1_2_6_3_1 doi: 10.1016/0304-3940(92)90065-F – ident: e_1_2_6_13_1 doi: 10.1016/j.neuroscience.2006.09.049 – ident: e_1_2_6_2_1 doi: 10.1113/jphysiol.2005.103820 – ident: e_1_2_6_16_1 doi: 10.1124/jpet.105.098467 – ident: e_1_2_6_10_1 doi: 10.1038/sj.bjp.0704413 – ident: e_1_2_6_22_1 doi: 10.1002/glia.20174 – ident: e_1_2_6_27_1 doi: 10.1046/j.1471-4159.1996.66041374.x – ident: e_1_2_6_7_1 doi: 10.1124/jpet.105.090787 – ident: e_1_2_6_29_1 doi: 10.1046/j.0953-816x.2001.01676.x |
| SSID | ssj0011497 |
| Score | 2.0826912 |
| Snippet | High concentrations of thrombin (Thr) have been linked to neuronal damage in cerebral ischemia and traumatic brain injury. In the present study we found that... |
| SourceID | proquest pubmed crossref wiley istex |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 917 |
| SubjectTerms | Animals Animals, Newborn astrocyte swelling Astrocytes - drug effects Astrocytes - metabolism Brain Damage, Chronic - metabolism Brain Damage, Chronic - physiopathology Brain Edema - metabolism Brain Edema - physiopathology Brain Injuries - metabolism Brain Injuries - physiopathology Brain Ischemia - metabolism Brain Ischemia - physiopathology Calcium Signaling - drug effects Calcium Signaling - physiology Cell Death - drug effects Cell Death - physiology Cells, Cultured DCPIB Enzyme Inhibitors - pharmacology Extracellular Fluid - metabolism Glutamic Acid - metabolism Hypotonic Solutions - pharmacology intracerebral hemorrhage Oligopeptides - pharmacology Osmotic Pressure - drug effects PAR-1 Rats Receptors, Thrombin - drug effects Receptors, Thrombin - metabolism Signal Transduction - drug effects Signal Transduction - physiology tamoxifen Thrombin - metabolism Thrombin - pharmacology volume-sensitive anion channel Water-Electrolyte Balance - drug effects Water-Electrolyte Balance - physiology |
| Title | Thrombin potently enhances swelling-sensitive glutamate efflux from cultured astrocytes |
| URI | https://api.istex.fr/ark:/67375/WNG-P9XS8NHN-N/fulltext.pdf https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fglia.20513 https://www.ncbi.nlm.nih.gov/pubmed/17437307 https://www.proquest.com/docview/20436436 https://www.proquest.com/docview/70556378 |
| Volume | 55 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Nb9QwELWq9sIFKOUjbSmWQJVAShvHThxLXFaIdkEQIWjFckCWE9st6jZbbbJSlxM_ob-RX8LY2WRVVJDglsNEcuw3nufJzDNCzyLOlYqFDm0W05BZkYYZ0yI0xgKkdBGXwvU7v8_T4TF7O0pGK-hl1wvT6kP0CTfnGX6_dg6uinp_KRp6Mv7mdIMSf2WtK9ZyjOhjrx0FPF-0Mp-ChfBMem3SeH_56rVotOYm9vImqnmdufrQc3AHfe0G3VacnO3NmmKv_P6bnuP_ftVddHvBSfGgBdE6WjHVPbQxqOA8fj7Hu9hXifr0-wb6cnQ6nZzDcRpfTIBuN-M5NtWpg06Na5cIhFD488dV7eri3U6KTwDaCmixwcba8ewSu4YW3Ap-GI1V3UAInQPhvY-OD14fvRqGi-sZwpKC24Y64ZYJRhTVES0JUTyNRJkIqgizPKacR6VWiguTUAY2pBRGwWkrBVKfZZTQB2i1mlTmEcJAS6kAcpSyLGEcEGNJoU2UGKGFsrEN0PNumWS50C53V2iMZau6HEs3b9LPW4Ce9rYXrWLHjVa7frV7EzU9czVuPJGf80P5QYw-Zfkwl3mAnnRwkOB57neKqsxkVkvXVQx8Lv2zhVcqojwL0MMWR8sBcScpFfEAvfBo-MtI5eG7NwP_tPkvxlvoVpeGjsg2Wm2mM_MY-FNT7Hg_-QX3QRcE |
| linkProvider | Wiley-Blackwell |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1fb9MwELfQ9gAv_BuwbIxZAk0CKVsSO3H8WE1sHXQRgk6UJ8tN7A2tS6cmlVae-Aj7jHyS3TltqqGBBG95uEiOfef73eXud4S8CYTQOpKFb9OI-dzKxE95IX1jLKhUMYxyif3Ox1nSPeEfBvFgXpuDvTANP0SbcEPLcPc1GjgmpPeWrKGno-9IHBTjzNpVHOntIqrPLXsUIH3ZEH1K7sNz2LKTRnvLd2_5o1Xc2qu7wOZt7Oqcz8GjZsJq5TgLsebkfHdaD3fzH78xOv73dz0mD-ewlHYaPXpC7pnyKVnrlBCSX8zoDnWFoi4Dv0a-9c8m4wuIqOnlGBB3PZpRU56h9lS0wlwgeMNfP68rLI3Hy5SegnZrQMaGGmtH0yuKPS204fwwBdVVDV50Bpj3GTk5eN_f7_rzCQ1-zsBy_SIWlksealYELA9DLZJA5rFkOuRWREyIIC-0FtLEjINMmEujIeBKANenKQvZc7JSjkuzTiggUyYBHyU8jbkApbHhsDBBbGQhtY2sR94uzknlc_pynKIxUg3xcqRw35TbN4-8bmUvG9KOO6V23HG3InpyjmVuIlZfs0P1SQ6-pFk3U5lHthf6oMD48I-KLs14WilsLAZIl_xZwpEVMZF65EWjSMsFCWSVCoRH3jl1-MtK1WHvqOOeNv5FeJvc7_aPe6p3lH3cJA8WWekgfElW6snUbAGcqoevnNHcAE43Gx8 |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Rb9MwELamTUK8sMGAhQGzBJoEUrYkduJY4qVidB2MaIJNlAdkubG9oXVp1aTSuqf9BH4jv4Sz06QaGkjwloeL5Njf-T5f7j4j9DJgTMqIK9-kEfGp4YmfUsV9rQ1ASg2inNt-549Z0juh7_txfwm9aXphan2INuFmPcPt19bBx8rsLkRDT4ffrW5QbK-sXaFJkFpM731qxaOA6PNa55NTH57DVpw02l28eyMcrdiZvbyNa96kri72dFfRt2bUdcnJ-c60GuzkV78JOv7vZ62he3NSijs1iu6jJV08QOudAg7kFzO8jV2ZqMu_r6Ovx2eT0QWcp_F4BHy7Gs6wLs4sdkpc2kwgxMKf1z9KWxhvt1J8CtiWwIs11sYMp5fYdrTgWvFDKyzLCmLoDBjvQ3TSfXf8tufP72fwcwJ-66uYGcppKIkKSB6GkiUBz2NOZEgNiwhjQa6kZFzHhIJNmHMt4biVAKtPUxKSR2i5GBV6A2HgpYQDO0poGlMGkDHhQOkg1lxxaSLjoVfNMol8Ll5u79AYilp2ORJ23oSbNw-9aG3HtWTHrVbbbrVbEzk5t0VuLBZfsn1xxPuf06yXicxDWw0cBLie_Z8iCz2alsK2FQOhS_5s4aSKCEs99LjG0WJAzGpKBcxDrx0a_jJSsX940HFPT_7FeAvdOdrrisOD7MMmutukpIPwKVquJlP9DLhUNXjuXOYXC90Z1w |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Thrombin+potently+enhances+swelling%E2%80%90sensitive+glutamate+efflux+from+cultured+astrocytes&rft.jtitle=Glia&rft.au=Ramos%E2%80%90Mandujano%2C+Gerardo&rft.au=V%C3%A1zquez%E2%80%90Ju%C3%A1rez%2C+Erika&rft.au=Hern%C3%A1ndez%E2%80%90Ben%C3%ADtez%2C+Reyna&rft.au=Pasantes%E2%80%90Morales%2C+Herminia&rft.date=2007-07-01&rft.issn=0894-1491&rft.eissn=1098-1136&rft.volume=55&rft.issue=9&rft.spage=917&rft.epage=925&rft_id=info:doi/10.1002%2Fglia.20513&rft.externalDBID=n%2Fa&rft.externalDocID=10_1002_glia_20513 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0894-1491&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0894-1491&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0894-1491&client=summon |