Tumor necrosis factor-α-induced TRPC1 expression amplifies store-operated Ca 2+ influx and endothelial permeability
We determined the effects of TNF-α on the expression of transient receptor potential channel (TRPC) homologues in human vascular endothelial cells and the consequences of TRPC expression on the endothelial permeability response. We observed that TNF-α exposure increased TRPC1 expression without sign...
Saved in:
Published in | American journal of physiology. Lung cellular and molecular physiology Vol. 287; no. 6; pp. L1303 - L1313 |
---|---|
Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
01.12.2004
|
Online Access | Get full text |
Cover
Loading…
Abstract | We determined the effects of TNF-α on the expression of transient receptor potential channel (TRPC) homologues in human vascular endothelial cells and the consequences of TRPC expression on the endothelial permeability response. We observed that TNF-α exposure increased TRPC1 expression without significantly altering expression of other TRPC isoforms in human pulmonary artery endothelial cells (HPAEC). Because TRPC1 belongs to the store-operated cation channel family, we measured the Ca
2+
store depletion-mediated Ca
2+
influx in response to thrombin exposure. We observed that thrombin-induced Ca
2+
influx in TNF-α-stimulated HPAEC was twofold greater than in control cells. To address the relationship between store-operated Ca
2+
influx and TRPC1 expression, we overexpressed TRPC1 by three- to fourfold in the human dermal microvascular endothelial cell line (HMEC) using the TRPC1 cDNA. Thrombin-induced store Ca
2+
depletion in these cells caused approximately twofold greater increase in Ca
2+
influx than in control cells. Furthermore, the inositol 1,4,5-trisphosphate-sensitive store-operated cationic current was increased greater than twofold in TRPC1-transfected cells compared with control. To address the role of Ca
2+
influx via TRPC1 in signaling endothelial permeability, we measured actin-stress fiber formation and transendothelial monolayer electrical resistance (TER) in the TRPC1 cDNA-transfected HMEC and TNF-α-challenged HPAEC. Both thrombin-induced actin-stress fiber formation and a decrease in TER were augmented in TRPC1-overexpressing HMEC compared with control cells. TNF-α-induced increased TRPC1 expression in HPAEC also resulted in marked endothelial barrier dysfunction in response to thrombin. These findings indicate the expression level of TRPC1 in endothelial cells is a critical determinant of Ca
2+
influx and signaling of the increase in endothelial permeability. |
---|---|
AbstractList | We determined the effects of TNF-α on the expression of transient receptor potential channel (TRPC) homologues in human vascular endothelial cells and the consequences of TRPC expression on the endothelial permeability response. We observed that TNF-α exposure increased TRPC1 expression without significantly altering expression of other TRPC isoforms in human pulmonary artery endothelial cells (HPAEC). Because TRPC1 belongs to the store-operated cation channel family, we measured the Ca
2+
store depletion-mediated Ca
2+
influx in response to thrombin exposure. We observed that thrombin-induced Ca
2+
influx in TNF-α-stimulated HPAEC was twofold greater than in control cells. To address the relationship between store-operated Ca
2+
influx and TRPC1 expression, we overexpressed TRPC1 by three- to fourfold in the human dermal microvascular endothelial cell line (HMEC) using the TRPC1 cDNA. Thrombin-induced store Ca
2+
depletion in these cells caused approximately twofold greater increase in Ca
2+
influx than in control cells. Furthermore, the inositol 1,4,5-trisphosphate-sensitive store-operated cationic current was increased greater than twofold in TRPC1-transfected cells compared with control. To address the role of Ca
2+
influx via TRPC1 in signaling endothelial permeability, we measured actin-stress fiber formation and transendothelial monolayer electrical resistance (TER) in the TRPC1 cDNA-transfected HMEC and TNF-α-challenged HPAEC. Both thrombin-induced actin-stress fiber formation and a decrease in TER were augmented in TRPC1-overexpressing HMEC compared with control cells. TNF-α-induced increased TRPC1 expression in HPAEC also resulted in marked endothelial barrier dysfunction in response to thrombin. These findings indicate the expression level of TRPC1 in endothelial cells is a critical determinant of Ca
2+
influx and signaling of the increase in endothelial permeability. |
Author | Tiruppathi, Chinnaswamy Alamgir, Setara Malik, Asrar B. Ahmmed, Gias U. Vogel, Stephen M. Shroff, Jennifer Paria, Biman C. |
Author_xml | – sequence: 1 givenname: Biman C. surname: Paria fullname: Paria, Biman C. organization: Department of Pharmacology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612 – sequence: 2 givenname: Stephen M. surname: Vogel fullname: Vogel, Stephen M. organization: Department of Pharmacology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612 – sequence: 3 givenname: Gias U. surname: Ahmmed fullname: Ahmmed, Gias U. organization: Department of Pharmacology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612 – sequence: 4 givenname: Setara surname: Alamgir fullname: Alamgir, Setara organization: Department of Pharmacology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612 – sequence: 5 givenname: Jennifer surname: Shroff fullname: Shroff, Jennifer organization: Department of Pharmacology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612 – sequence: 6 givenname: Asrar B. surname: Malik fullname: Malik, Asrar B. organization: Department of Pharmacology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612 – sequence: 7 givenname: Chinnaswamy surname: Tiruppathi fullname: Tiruppathi, Chinnaswamy organization: Department of Pharmacology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612 |
BookMark | eNotkN9KwzAUxoNMcJu-gFe5l8yTNF3TSyn-g4EivS9pc6IZbVqSFrbH8kV8Jjvd1fng_Pjg-63IwvceCbnlsOE8Ffd6P7ST_9wACAkbASAvyHJ-CMZTkIs5gwQGW0ivyCrGPQCkANslGcup6wP12IQ-ukitbsY-sJ9v5ryZGjS0_HgvOMXDEDBG13uqu6F11mGkcUaR9QMGPc5koam4o87bdjpQ7Q1Fb_rxC1unWzpDHeratW48XpNLq9uIN-e7JuXTY1m8sN3b82vxsGNNLiRTuUx0bTValYE0QltUjeBZrUFoZXJVpybPLNRJhirTKjcqscClEDwRCSbJmoj_2tO2GNBWQ3CdDseKQ3XSVp21VX_aqpO25Bcrp2au |
CitedBy_id | crossref_primary_10_1159_000513644 crossref_primary_10_1152_ajplung_00458_2015 crossref_primary_10_1152_ajpcell_00470_2008 crossref_primary_10_1016_j_ceca_2012_07_001 crossref_primary_10_1080_21688370_2017_1331722 crossref_primary_10_1016_j_bbadis_2007_02_013 crossref_primary_10_3390_cells9010135 crossref_primary_10_1089_scd_2010_0047 crossref_primary_10_1074_jbc_M112_411272 crossref_primary_10_1007_s12264_023_01151_5 crossref_primary_10_1007_s00018_011_0755_x crossref_primary_10_1016_j_ceca_2005_06_028 crossref_primary_10_1016_j_bcp_2009_04_029 crossref_primary_10_1083_jcb_201504038 crossref_primary_10_1080_10739680600930313 crossref_primary_10_1111_cpf_12787 crossref_primary_10_1084_jem_20150353 crossref_primary_10_1086_677356 crossref_primary_10_1016_j_semcdb_2006_10_010 crossref_primary_10_1016_j_ceca_2019_102061 crossref_primary_10_1016_j_bbamem_2007_11_007 crossref_primary_10_1016_j_freeradbiomed_2019_08_018 crossref_primary_10_1152_ajplung_00555_2016 crossref_primary_10_3390_cells7070070 crossref_primary_10_1074_jbc_M110_214940 crossref_primary_10_1002_jbt_22463 crossref_primary_10_1089_scd_2011_0027 crossref_primary_10_3389_fphys_2020_00421 crossref_primary_10_1016_j_ceca_2015_01_002 crossref_primary_10_1161_CIRCRESAHA_112_269506 crossref_primary_10_3389_fphys_2021_645109 crossref_primary_10_3389_fcvm_2020_602183 crossref_primary_10_3390_cells10071654 crossref_primary_10_1111_imr_12443 crossref_primary_10_1016_j_pharmthera_2008_03_008 crossref_primary_10_3390_biom12040484 crossref_primary_10_1152_physrev_00026_2014 crossref_primary_10_1016_j_peptides_2020_170297 crossref_primary_10_1016_j_cyto_2020_155066 crossref_primary_10_1007_s11427_014_4713_3 crossref_primary_10_1016_j_peptides_2009_04_007 crossref_primary_10_1053_j_semtcvs_2006_09_004 crossref_primary_10_3390_cells3040939 crossref_primary_10_1016_j_drudis_2006_08_002 crossref_primary_10_1097_MEG_0000000000002034 crossref_primary_10_1080_19336950_2021_1983100 crossref_primary_10_1016_j_ceca_2011_08_006 crossref_primary_10_1177_0271678X231216270 crossref_primary_10_1152_ajpcell_00280_2011 crossref_primary_10_1096_fj_08_119495 crossref_primary_10_1021_acs_jafc_9b03079 crossref_primary_10_1038_bjp_2008_141 crossref_primary_10_1113_JP276245 crossref_primary_10_1080_10739680600930347 crossref_primary_10_1074_jbc_M114_570051 crossref_primary_10_3389_fimmu_2023_1127277 crossref_primary_10_1016_j_bbamcr_2017_06_001 crossref_primary_10_1586_ecp_10_15 crossref_primary_10_1016_j_yjmcc_2012_07_002 crossref_primary_10_2500_ajr_2008_22_3125 crossref_primary_10_1080_10739680802220323 crossref_primary_10_1007_s12035_018_1213_7 crossref_primary_10_1113_JP272844 crossref_primary_10_1089_ars_2010_3740 crossref_primary_10_1080_10739680600930354 crossref_primary_10_2139_ssrn_3721693 crossref_primary_10_1096_fj_15_275891 crossref_primary_10_1098_rstb_2013_0103 crossref_primary_10_1016_S1016_8478_23_12859_7 crossref_primary_10_1074_jbc_M600722200 crossref_primary_10_1042_BJ20060124 crossref_primary_10_1016_j_ceca_2016_12_009 crossref_primary_10_1016_j_vph_2015_06_005 crossref_primary_10_1124_mol_111_074658 crossref_primary_10_1016_j_theriogenology_2016_02_005 crossref_primary_10_1016_j_ceca_2006_08_011 crossref_primary_10_1177_2045893217752912 crossref_primary_10_12659_MSM_901920 crossref_primary_10_1038_s41598_018_30625_0 crossref_primary_10_1074_jbc_M112_361139 crossref_primary_10_1016_j_ceca_2016_02_002 crossref_primary_10_1152_ajpheart_00457_2014 crossref_primary_10_1159_000512618 crossref_primary_10_1124_jpet_112_196832 crossref_primary_10_3233_CH_242281 crossref_primary_10_1152_ajpcell_00218_2015 crossref_primary_10_1038_s41598_020_61177_x crossref_primary_10_1111_j_1476_5381_2010_00985_x crossref_primary_10_1016_j_ceca_2007_01_013 crossref_primary_10_3390_ijms24044087 crossref_primary_10_1007_s00424_005_1465_8 crossref_primary_10_1111_j_1440_1681_2006_04394_x crossref_primary_10_1165_rcmb_2006_0003OC crossref_primary_10_12677_AMB_2015_44009 crossref_primary_10_4103_2045_8932_109920 crossref_primary_10_1016_j_bbadis_2007_02_009 crossref_primary_10_1038_nrc1628 crossref_primary_10_1186_s13046_018_0714_6 crossref_primary_10_1196_annals_1420_016 |
Cites_doi | 10.1016/S0014-5793(98)01212-5 10.1152/physrev.2001.81.4.1415 10.1126/science.287.5458.1647 10.1006/abio.2001.5458 10.1152/ajpcell.1999.276.1.C38 10.1038/24890 10.1016/S0021-9258(18)83649-3 10.1152/ajpcell.1999.276.4.C969 10.1152/ajplung.1998.275.3.L574 10.1152/ajplung.2001.281.4.L958 10.1084/jem.163.3.740 10.1073/pnas.97.13.7440 10.1152/ajplung.1992.263.2.L219 10.1161/01.RES.0000023391.40106.A8 10.1152/ajplung.2001.280.2.L239 10.1074/jbc.M306705200 10.1152/physiologyonline.1998.13.5.211 10.1016/S0092-8674(02)00670-0 10.1152/ajplung.2001.281.5.L1037 10.1038/35055019 10.1152/ajplung.1994.267.3.L223 10.1073/pnas.93.26.15195 10.1074/jbc.274.19.13718 10.1074/jbc.275.5.3403 10.1073/pnas.102596199 10.1073/pnas.96.26.14669 10.1016/S0143-4160(03)00068-X 10.1172/JCI115681 10.1056/NEJM200103083441009 10.1016/S1537-1891(03)00007-7 10.1056/NEJM200005043421806 10.1111/j.1469-7793.2001.0433a.x 10.1073/pnas.89.17.7919 10.1152/physiolgenomics.2000.4.2.137 10.1002/jez.1073 10.1074/jbc.M304287200 10.1152/jappl.2001.91.4.1487 10.1046/j.1538-7836.2003.00261.x 10.1074/jbc.M302983200 10.1159/000016321 |
ContentType | Journal Article |
DBID | AAYXX CITATION |
DOI | 10.1152/ajplung.00240.2004 |
DatabaseName | CrossRef |
DatabaseTitle | CrossRef |
DatabaseTitleList | CrossRef |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Anatomy & Physiology Chemistry Biology |
EISSN | 1522-1504 |
EndPage | L1313 |
ExternalDocumentID | 10_1152_ajplung_00240_2004 |
GroupedDBID | --- 23M 2WC 39C 4.4 53G 5GY 5VS 8M5 AAYXX ACPRK ADBBV AENEX AFFNX AFRAH ALMA_UNASSIGNED_HOLDINGS BAWUL BKKCC BKOMP BTFSW C1A CITATION DIK E3Z EBS EJD EMOBN F5P H13 ITBOX KQ8 OK1 P2P PQQKQ RAP RHF RHI RPL RPRKH TR2 W8F WH7 WOQ XSW YSK |
ID | FETCH-LOGICAL-c924-8943abfaef8704d2afe8c217ba02a8d98b5d97f0b37e87a89d83f014221323e33 |
ISSN | 1040-0605 |
IngestDate | Fri Aug 23 00:23:31 EDT 2024 |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 6 |
Language | English |
LinkModel | OpenURL |
MergedId | FETCHMERGED-LOGICAL-c924-8943abfaef8704d2afe8c217ba02a8d98b5d97f0b37e87a89d83f014221323e33 |
ParticipantIDs | crossref_primary_10_1152_ajplung_00240_2004 |
PublicationCentury | 2000 |
PublicationDate | 2004-12-00 |
PublicationDateYYYYMMDD | 2004-12-01 |
PublicationDate_xml | – month: 12 year: 2004 text: 2004-12-00 |
PublicationDecade | 2000 |
PublicationTitle | American journal of physiology. Lung cellular and molecular physiology |
PublicationYear | 2004 |
References | R41 R40 R21 R20 R42 R23 R22 R25 R24 R27 R26 R29 R28 R1 R2 R3 R4 R5 R6 R7 R8 R9 R30 R10 R32 R31 R12 R34 R11 R33 R14 R36 R13 R35 R16 R38 R15 R37 R18 R17 R39 R19 |
References_xml | – ident: R15 doi: 10.1016/S0014-5793(98)01212-5 – ident: R27 doi: 10.1152/physrev.2001.81.4.1415 – ident: R22 doi: 10.1126/science.287.5458.1647 – ident: R39 doi: 10.1006/abio.2001.5458 – ident: R7 doi: 10.1152/ajpcell.1999.276.1.C38 – ident: R17 doi: 10.1038/24890 – ident: R8 doi: 10.1016/S0021-9258(18)83649-3 – ident: R40 doi: 10.1152/ajpcell.1999.276.4.C969 – ident: R25 doi: 10.1152/ajplung.1998.275.3.L574 – ident: R36 doi: 10.1152/ajplung.2001.281.4.L958 – ident: R26 doi: 10.1084/jem.163.3.740 – ident: R37 doi: 10.1073/pnas.97.13.7440 – ident: R20 doi: 10.1152/ajplung.1992.263.2.L219 – ident: R33 doi: 10.1161/01.RES.0000023391.40106.A8 – ident: R31 doi: 10.1152/ajplung.2001.280.2.L239 – ident: R32 doi: 10.1074/jbc.M306705200 – ident: R42 doi: 10.1152/physiologyonline.1998.13.5.211 – ident: R24 doi: 10.1016/S0092-8674(02)00670-0 – ident: R11 doi: 10.1152/ajplung.2001.281.5.L1037 – ident: R14 doi: 10.1038/35055019 – ident: R21 doi: 10.1152/ajplung.1994.267.3.L223 – ident: R2 doi: 10.1073/pnas.93.26.15195 – ident: R10 – ident: R6 doi: 10.1074/jbc.274.19.13718 – ident: R18 doi: 10.1074/jbc.275.5.3403 – ident: R5 – ident: R16 doi: 10.1073/pnas.102596199 – ident: R29 doi: 10.1073/pnas.96.26.14669 – ident: R1 doi: 10.1016/S0143-4160(03)00068-X – ident: R19 doi: 10.1172/JCI115681 – ident: R23 doi: 10.1056/NEJM200103083441009 – ident: R35 doi: 10.1016/S1537-1891(03)00007-7 – ident: R41 doi: 10.1056/NEJM200005043421806 – ident: R30 doi: 10.1111/j.1469-7793.2001.0433a.x – ident: R34 doi: 10.1073/pnas.89.17.7919 – ident: R38 doi: 10.1152/physiolgenomics.2000.4.2.137 – ident: R12 doi: 10.1002/jez.1073 – ident: R28 doi: 10.1074/jbc.M304287200 – ident: R4 doi: 10.1152/jappl.2001.91.4.1487 – ident: R9 doi: 10.1046/j.1538-7836.2003.00261.x – ident: R3 doi: 10.1074/jbc.M302983200 – ident: R13 doi: 10.1159/000016321 |
SSID | ssj0005006 |
Score | 1.7845881 |
Snippet | We determined the effects of TNF-α on the expression of transient receptor potential channel (TRPC) homologues in human vascular endothelial cells and the... |
SourceID | crossref |
SourceType | Aggregation Database |
StartPage | L1303 |
Title | Tumor necrosis factor-α-induced TRPC1 expression amplifies store-operated Ca 2+ influx and endothelial permeability |
Volume | 287 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3NjtMwELbKIgQXBLsg_uUD5RKlJI7TJsc2WljBLlpQF-2tchJ7CWrSqptIwFvxIjwHj8GMnb9SkFgOjdLYstrMJ49n5psZQp57KubpxGN2onzf5r5y7VAKZseu5wuRKBWOMVH45N346Iy_OffPB4OfPdZSVcaj5Nsf80r-R6rwDOSKWbJXkGy7KDyAe5AvXEHCcP03GVf5amMVElVddln3zrGH0eFw5tpgbFcY3J9_OI1crORvGK-FJZBErsBCtpAZKe3VGgsro6dXWGzIZkjQWlZfdFhBFimmaC3Rrw7TcmnKem_FgtugT68KhXaYaI_9yDquMK9XLpea8Yqr5k1P3t68Lpa1MfzdWYbhhWjUDHxcXRhGQU1Ms07aoemnPDdO29eZuLTOugHA-0VmWovJUmzElpOD9wgjZl9G4qMzdkwAXNZ7NdjRcJ7l_c2c1eo729maj1Fb9_Q8fDdZsLtKxMeitOLzegnvZ6SrwGlHQqcyG5rAb5q05Tdqy8pni3qNhV4DO37ya-Q6m4Q-kk_fvu_q2vuO7gLb_s0mvctnL3d_R-8I1TsLze-Q27URQ6cGkXfJQBb75GBaiHKVf6Uv6Gkr1X1yY9bc3Yya5oIHpNTQpQ10aQ3dH98b2FINW9rBlrawpduwpZGgzKIGtBTgRXugpX3Q3iPzV4fz6MiuG4DYSci4ja0BRKyEVKBUeMqEkkECJnQsHCaCNAxiPw0nyom9iQwmIgjTwFMOOjVdj3nS8-6TvWJVyAeEeoqPFSziwNGE8yQIQtiMVCBCVwbwSR8Sq3mli7Up87L4uxAfXWn2Y3Krg_QTslduKvkUTrJl_EyD4BcMx6Lz |
link.rule.ids | 315,786,790,27955,27956 |
linkProvider | Colorado Alliance of Research Libraries |
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=Tumor+necrosis+factor-%CE%B1-induced+TRPC1+expression+amplifies+store-operated+Ca+2%2B+influx+and+endothelial+permeability&rft.jtitle=American+journal+of+physiology.+Lung+cellular+and+molecular+physiology&rft.au=Paria%2C+Biman+C.&rft.au=Vogel%2C+Stephen+M.&rft.au=Ahmmed%2C+Gias+U.&rft.au=Alamgir%2C+Setara&rft.date=2004-12-01&rft.issn=1040-0605&rft.eissn=1522-1504&rft.volume=287&rft.issue=6&rft.spage=L1303&rft.epage=L1313&rft_id=info:doi/10.1152%2Fajplung.00240.2004&rft.externalDBID=n%2Fa&rft.externalDocID=10_1152_ajplung_00240_2004 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1040-0605&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1040-0605&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1040-0605&client=summon |