Pro-inflammatory gene expression and neurotoxic effects of activated microglia are attenuated by absence of CCAAT/enhancer binding protein β
Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial activation or neuroinflammation, can be detrimental to the surrounding tissue. The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) is an important regul...
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Published in | Journal of neuroinflammation Vol. 8; no. 1; p. 156 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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BioMed Central Ltd
10.11.2011
BioMed Central BMC |
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Abstract | Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial activation or neuroinflammation, can be detrimental to the surrounding tissue. The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) is an important regulator of gene expression in inflammation but little is known about its involvement in glial activation. To explore the functional role of C/EBPβ in glial activation we have analyzed pro-inflammatory gene expression and neurotoxicity in murine wild type and C/EBPβ-null glial cultures.
Due to fertility and mortality problems associated with the C/EBPβ-null genotype we developed a protocol to prepare mixed glial cultures from cerebral cortex of a single mouse embryo with high yield. Wild-type and C/EBPβ-null glial cultures were compared in terms of total cell density by Hoechst-33258 staining; microglial content by CD11b immunocytochemistry; astroglial content by GFAP western blot; gene expression by quantitative real-time PCR, western blot, immunocytochemistry and Griess reaction; and microglial neurotoxicity by estimating MAP2 content in neuronal/microglial cocultures. C/EBPβ DNA binding activity was evaluated by electrophoretic mobility shift assay and quantitative chromatin immunoprecipitation.
C/EBPβ mRNA and protein levels, as well as DNA binding, were increased in glial cultures by treatment with lipopolysaccharide (LPS) or LPS + interferon γ (IFNγ). Quantitative chromatin immunoprecipitation showed binding of C/EBPβ to pro-inflammatory gene promoters in glial activation in a stimulus- and gene-dependent manner. In agreement with these results, LPS and LPS+IFNγ induced different transcriptional patterns between pro-inflammatory cytokines and NO synthase-2 genes. Furthermore, the expressions of IL-1β and NO synthase-2, and consequent NO production, were reduced in the absence of C/EBPβ. In addition, neurotoxicity elicited by LPS+IFNγ-treated microglia co-cultured with neurons was completely abolished by the absence of C/EBPβ in microglia.
These findings show involvement of C/EBPβ in the regulation of pro-inflammatory gene expression in glial activation, and demonstrate for the first time a key role for C/EBPβ in the induction of neurotoxic effects by activated microglia. |
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AbstractList | Abstract Background Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial activation or neuroinflammation, can be detrimental to the surrounding tissue. The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) is an important regulator of gene expression in inflammation but little is known about its involvement in glial activation. To explore the functional role of C/EBPβ in glial activation we have analyzed pro-inflammatory gene expression and neurotoxicity in murine wild type and C/EBPβ-null glial cultures. Methods Due to fertility and mortality problems associated with the C/EBPβ-null genotype we developed a protocol to prepare mixed glial cultures from cerebral cortex of a single mouse embryo with high yield. Wild-type and C/EBPβ-null glial cultures were compared in terms of total cell density by Hoechst-33258 staining; microglial content by CD11b immunocytochemistry; astroglial content by GFAP western blot; gene expression by quantitative real-time PCR, western blot, immunocytochemistry and Griess reaction; and microglial neurotoxicity by estimating MAP2 content in neuronal/microglial cocultures. C/EBPβ DNA binding activity was evaluated by electrophoretic mobility shift assay and quantitative chromatin immunoprecipitation. Results C/EBPβ mRNA and protein levels, as well as DNA binding, were increased in glial cultures by treatment with lipopolysaccharide (LPS) or LPS + interferon γ (IFNγ). Quantitative chromatin immunoprecipitation showed binding of C/EBPβ to pro-inflammatory gene promoters in glial activation in a stimulus- and gene-dependent manner. In agreement with these results, LPS and LPS+IFNγ induced different transcriptional patterns between pro-inflammatory cytokines and NO synthase-2 genes. Furthermore, the expressions of IL-1β and NO synthase-2, and consequent NO production, were reduced in the absence of C/EBPβ. In addition, neurotoxicity elicited by LPS+IFNγ-treated microglia co-cultured with neurons was completely abolished by the absence of C/EBPβ in microglia. Conclusions These findings show involvement of C/EBPβ in the regulation of pro-inflammatory gene expression in glial activation, and demonstrate for the first time a key role for C/EBPβ in the induction of neurotoxic effects by activated microglia. Background. Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial activation or neuroinflammation, can be detrimental to the surrounding tissue. The transcription factor CCAAT/enhancer binding protein ß (C/EBPß) is an important regulator of gene expression in inflammation but little is known about its involvement in glial activation. To explore the functional role of C/EBPß in glial activation we have analyzed pro-inflammatory gene expression and neurotoxicity in murine wild type and C/EBPß-null glial cultures. Methods. Due to fertility and mortality problems associated with the C/EBPß-null genotype we developed a protocol to prepare mixed glial cultures from cerebral cortex of a single mouse embryo with high yield. Wild-type and C/EBPß-null glial cultures were compared in terms of total cell density by Hoechst-33258 staining; microglial content by CD11b immunocytochemistry; astroglial content by GFAP western blot; gene expression by quantitative real-time PCR, western blot, immunocytochemistry and Griess reaction; and microglial neurotoxicity by estimating MAP2 content in neuronal/microglial cocultures. C/EBPß DNA binding activity was evaluated by electrophoretic mobility shift assay and quantitative chromatin immunoprecipitation. Results. C/EBPß mRNA and protein levels, as well as DNA binding, were increased in glial cultures by treatment with lipopolysaccharide (LPS) or LPS + interferon ¿ (IFN¿). Quantitative chromatin immunoprecipitation showed binding of C/EBPß to pro-inflammatory gene promoters in glial activation in a stimulus- and gene-dependent manner. In agreement with these results, LPS and LPS+IFN¿ induced different transcriptional patterns between pro-inflammatory cytokines and NO synthase-2 genes. Furthermore, the expressions of IL-1ß and NO synthase-2, and consequent NO production, were reduced in the absence of C/EBPß. In addition, neurotoxicity elicited by LPS+IFN¿-treated microglia co-cultured with neurons was completely abolished by the absence of C/EBPß in microglia. BACKGROUND: Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial activation or neuroinflammation, can be detrimental to the surrounding tissue. The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) is an important regulator of gene expression in inflammation but little is known about its involvement in glial activation. To explore the functional role of C/EBPβ in glial activation we have analyzed pro-inflammatory gene expression and neurotoxicity in murine wild type and C/EBPβ-null glial cultures. METHODS: Due to fertility and mortality problems associated with the C/EBPβ-null genotype we developed a protocol to prepare mixed glial cultures from cerebral cortex of a single mouse embryo with high yield. Wild-type and C/EBPβ-null glial cultures were compared in terms of total cell density by Hoechst-33258 staining; microglial content by CD11b immunocytochemistry; astroglial content by GFAP western blot; gene expression by quantitative real-time PCR, western blot, immunocytochemistry and Griess reaction; and microglial neurotoxicity by estimating MAP2 content in neuronal/microglial cocultures. C/EBPβ DNA binding activity was evaluated by electrophoretic mobility shift assay and quantitative chromatin immunoprecipitation. RESULTS: C/EBPβ mRNA and protein levels, as well as DNA binding, were increased in glial cultures by treatment with lipopolysaccharide (LPS) or LPS + interferon γ (IFNγ). Quantitative chromatin immunoprecipitation showed binding of C/EBPβ to pro-inflammatory gene promoters in glial activation in a stimulus- and gene-dependent manner. In agreement with these results, LPS and LPS+IFNγ induced different transcriptional patterns between pro-inflammatory cytokines and NO synthase-2 genes. Furthermore, the expressions of IL-1β and NO synthase-2, and consequent NO production, were reduced in the absence of C/EBPβ. In addition, neurotoxicity elicited by LPS+IFNγ-treated microglia co-cultured with neurons was completely abolished by the absence of C/EBPβ in microglia. CONCLUSIONS: These findings show involvement of C/EBPβ in the regulation of pro-inflammatory gene expression in glial activation, and demonstrate for the first time a key role for C/EBPβ in the induction of neurotoxic effects by activated microglia. Abstract Background Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial activation or neuroinflammation, can be detrimental to the surrounding tissue. The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) is an important regulator of gene expression in inflammation but little is known about its involvement in glial activation. To explore the functional role of C/EBPβ in glial activation we have analyzed pro-inflammatory gene expression and neurotoxicity in murine wild type and C/EBPβ-null glial cultures. Methods Due to fertility and mortality problems associated with the C/EBPβ-null genotype we developed a protocol to prepare mixed glial cultures from cerebral cortex of a single mouse embryo with high yield. Wild-type and C/EBPβ-null glial cultures were compared in terms of total cell density by Hoechst-33258 staining; microglial content by CD11b immunocytochemistry; astroglial content by GFAP western blot; gene expression by quantitative real-time PCR, western blot, immunocytochemistry and Griess reaction; and microglial neurotoxicity by estimating MAP2 content in neuronal/microglial cocultures. C/EBPβ DNA binding activity was evaluated by electrophoretic mobility shift assay and quantitative chromatin immunoprecipitation. Results C/EBPβ mRNA and protein levels, as well as DNA binding, were increased in glial cultures by treatment with lipopolysaccharide (LPS) or LPS + interferon γ (IFNγ). Quantitative chromatin immunoprecipitation showed binding of C/EBPβ to pro-inflammatory gene promoters in glial activation in a stimulus- and gene-dependent manner. In agreement with these results, LPS and LPS+IFNγ induced different transcriptional patterns between pro-inflammatory cytokines and NO synthase-2 genes. Furthermore, the expressions of IL-1β and NO synthase-2, and consequent NO production, were reduced in the absence of C/EBPβ. In addition, neurotoxicity elicited by LPS+IFNγ-treated microglia co-cultured with neurons was completely abolished by the absence of C/EBPβ in microglia. Conclusions These findings show involvement of C/EBPβ in the regulation of pro-inflammatory gene expression in glial activation, and demonstrate for the first time a key role for C/EBPβ in the induction of neurotoxic effects by activated microglia. Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial activation or neuroinflammation, can be detrimental to the surrounding tissue. The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) is an important regulator of gene expression in inflammation but little is known about its involvement in glial activation. To explore the functional role of C/EBPβ in glial activation we have analyzed pro-inflammatory gene expression and neurotoxicity in murine wild type and C/EBPβ-null glial cultures. Due to fertility and mortality problems associated with the C/EBPβ-null genotype we developed a protocol to prepare mixed glial cultures from cerebral cortex of a single mouse embryo with high yield. Wild-type and C/EBPβ-null glial cultures were compared in terms of total cell density by Hoechst-33258 staining; microglial content by CD11b immunocytochemistry; astroglial content by GFAP western blot; gene expression by quantitative real-time PCR, western blot, immunocytochemistry and Griess reaction; and microglial neurotoxicity by estimating MAP2 content in neuronal/microglial cocultures. C/EBPβ DNA binding activity was evaluated by electrophoretic mobility shift assay and quantitative chromatin immunoprecipitation. C/EBPβ mRNA and protein levels, as well as DNA binding, were increased in glial cultures by treatment with lipopolysaccharide (LPS) or LPS + interferon γ (IFNγ). Quantitative chromatin immunoprecipitation showed binding of C/EBPβ to pro-inflammatory gene promoters in glial activation in a stimulus- and gene-dependent manner. In agreement with these results, LPS and LPS+IFNγ induced different transcriptional patterns between pro-inflammatory cytokines and NO synthase-2 genes. Furthermore, the expressions of IL-1β and NO synthase-2, and consequent NO production, were reduced in the absence of C/EBPβ. In addition, neurotoxicity elicited by LPS+IFNγ-treated microglia co-cultured with neurons was completely abolished by the absence of C/EBPβ in microglia. These findings show involvement of C/EBPβ in the regulation of pro-inflammatory gene expression in glial activation, and demonstrate for the first time a key role for C/EBPβ in the induction of neurotoxic effects by activated microglia. |
ArticleNumber | 156 |
Author | Straccia, Marco Gresa-Arribas, Núria Tusell, Josep M Solà, Carme Ejarque-Ortiz, Aroa Serratosa, Joan Dentesano, Guido Saura, Josep |
AuthorAffiliation | 1 Biochemistry and Molecular Biology Unit, School of Medicine, University of Barcelona, IDIBAPS, Barcelona, Spain 2 Department of Brain Ischemia and Neurodegeneration, IIBB-CSIC, IDIBAPS, Barcelona, Spain |
AuthorAffiliation_xml | – name: 1 Biochemistry and Molecular Biology Unit, School of Medicine, University of Barcelona, IDIBAPS, Barcelona, Spain – name: 2 Department of Brain Ischemia and Neurodegeneration, IIBB-CSIC, IDIBAPS, Barcelona, Spain |
Author_xml | – sequence: 1 givenname: Marco surname: Straccia fullname: Straccia, Marco organization: Biochemistry and Molecular Biology Unit, School of Medicine, University of Barcelona, IDIBAPS, Barcelona, Spain – sequence: 2 givenname: Núria surname: Gresa-Arribas fullname: Gresa-Arribas, Núria – sequence: 3 givenname: Guido surname: Dentesano fullname: Dentesano, Guido – sequence: 4 givenname: Aroa surname: Ejarque-Ortiz fullname: Ejarque-Ortiz, Aroa – sequence: 5 givenname: Josep M surname: Tusell fullname: Tusell, Josep M – sequence: 6 givenname: Joan surname: Serratosa fullname: Serratosa, Joan – sequence: 7 givenname: Carme surname: Solà fullname: Solà, Carme – sequence: 8 givenname: Josep surname: Saura fullname: Saura, Josep |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22074460$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1038/nn1997 10.1186/1742-2094-8-34 10.1212/WNL.0b013e31820f2d79 10.1074/jbc.M108282200 10.1523/JNEUROSCI.06-08-02163.1986 10.1111/j.1471-4159.2006.03752.x 10.1111/j.1471-4159.2006.04056.x 10.1523/JNEUROSCI.23-08-03394.2003 10.1002/glia.10331 10.1523/JNEUROSCI.16-03-00919.1996 10.1186/1742-2094-4-26 10.1016/j.jneuroim.2006.01.014 10.1016/j.neuint.2006.04.003 10.1073/pnas.90.20.9730 10.1016/j.neulet.2006.09.078 10.1006/meth.2001.1262 10.1084/jem.189.4.719 10.1002/(SICI)1098-1136(20000101)29:1<91::AID-GLIA9>3.0.CO;2-I 10.1101/gad.11.17.2153 10.1371/journal.pone.0009516 10.1016/j.jneuroim.2009.02.003 10.1074/jbc.273.45.29279 10.1016/S1357-2725(97)00083-6 10.1016/j.bbrc.2008.04.055 10.1002/ana.20682 10.1523/JNEUROSCI.22-09-03484.2002 10.1111/j.1471-4159.2010.06952.x 10.4049/jimmunol.151.4.2132 10.1073/pnas.1007816107 10.1016/j.ceb.2008.02.002 10.1093/brain/awn230 10.1523/JNEUROSCI.5321-06.2007 10.1046/j.1471-4159.1998.70062424.x 10.1002/glia.21071 10.1046/j.1460-9568.2002.02199.x 10.1074/jbc.M800604200 10.1002/j.1460-2075.1995.tb07185.x 10.1016/S0197-4580(00)00241-4 10.1074/jbc.M203885200 10.1002/glia.20446 10.1038/70978 10.1046/j.1471-4159.2003.01788.x 10.1172/JCI3135 10.1096/fj.04-2591hyp 10.1016/j.imbio.2006.05.007 10.1111/j.1471-4159.2005.03395.x 10.1242/jcs.025031 10.1128/MCB.23.14.4841-4858.2003 10.1016/j.cell.2010.02.016 10.1128/MCB.19.3.1695 10.1042/bj20020508 10.4049/jimmunol.171.2.821 10.1111/j.1471-4159.2010.06928.x 10.1093/emboj/cdg076 10.1074/jbc.275.5.3107 10.4049/jimmunol.168.8.4055 10.1073/pnas.90.17.8219 10.1016/j.bbamcr.2005.05.009 10.1002/glia.10274 10.1002/jnr.22272 |
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References | 16753239 - Neurochem Int. 2006 Jul;49(2):183-9 8367486 - Proc Natl Acad Sci U S A. 1993 Sep 1;90(17):8219-23 18358708 - Curr Opin Cell Biol. 2008 Apr;20(2):180-5 16240369 - Ann Neurol. 2005 Dec;58(6):963-7 18339625 - J Biol Chem. 2008 May 9;283(19):13077-86 7744000 - EMBO J. 1995 May 1;14(9):1932-41 12716947 - J Neurosci. 2003 Apr 15;23(8):3394-406 16899075 - J Neurochem. 2006 Sep;98(6):1718-31 8558260 - J Neurosci. 1996 Feb 1;16(3):919-29 9603207 - J Neurochem. 1998 Jun;70(6):2424-33 11378246 - Neurobiol Aging. 2001 May-Jun;22(3):407-12 12405988 - Eur J Neurosci. 2002 Oct;16(7):1275-83 12787065 - J Neurochem. 2003 Jun;85(6):1455-67 14730702 - Glia. 2004 Feb;45(3):287-96 16504308 - J Neuroimmunol. 2006 May;174(1-2):63-73 12574124 - EMBO J. 2003 Feb 17;22(4):882-92 20878769 - Glia. 2011 Jan;59(1):1-13 20722966 - J Neurochem. 2010 Oct;115(2):526-36 10652293 - J Biol Chem. 2000 Feb 4;275(5):3107-13 21368281 - Neurology. 2011 Mar 8;76(10):863-9 10022857 - Mol Cell Biol. 1999 Mar;19(3):1695-704 9727068 - J Clin Invest. 1998 Sep 1;102(5):996-1007 11937564 - J Immunol. 2002 Apr 15;168(8):4055-62 20209087 - PLoS One. 2010;5(3):e9516 11668179 - J Biol Chem. 2001 Dec 28;276(52):48693-701 3018187 - J Neurosci. 1986 Aug;6(8):2163-78 18819987 - Brain. 2008 Nov;131(Pt 11):3019-33 20303880 - Cell. 2010 Mar 19;140(6):918-34 12832471 - Mol Cell Biol. 2003 Jul;23(14):4841-58 17965659 - Nat Neurosci. 2007 Nov;10(11):1387-94 11978825 - J Neurosci. 2002 May 1;22(9):3484-92 14603460 - Glia. 2003 Dec;44(3):183-9 10594926 - Glia. 2000 Jan 1;29(1):91-7 12847250 - J Immunol. 2003 Jul 15;171(2):821-8 15993497 - Biochim Biophys Acta. 2005 Sep 30;1745(3):287-99 8102159 - J Immunol. 1993 Aug 15;151(4):2132-41 18388310 - J Cell Sci. 2008 Apr 15;121(Pt 8):1224-34 10581083 - Nat Med. 1999 Dec;5(12):1403-9 9792624 - J Biol Chem. 1998 Nov 6;273(45):29279-82 9303532 - Genes Dev. 1997 Sep 1;11(17):2153-62 7692452 - Proc Natl Acad Sci U S A. 1993 Oct 15;90(20):9730-4 20974955 - Proc Natl Acad Sci U S A. 2010 Nov 9;107(45):19438-43 11846609 - Methods. 2001 Dec;25(4):402-8 16920490 - Immunobiology. 2006;211(6-8):511-24 21492414 - J Neuroinflammation. 2011;8:34 17937799 - J Neuroinflammation. 2007;4:26 17070994 - Neurosci Lett. 2006 Dec 13;410(1):25-30 17078024 - Glia. 2007 Jan 15;55(2):178-88 17376993 - J Neurosci. 2007 Mar 21;27(12):3328-37 12191995 - J Biol Chem. 2002 Oct 25;277(43):40594-601 9989987 - J Exp Med. 1999 Feb 15;189(4):719-27 15985529 - FASEB J. 2005 Jul;19(9):1061-6 20666933 - J Neurochem. 2010 Oct;115(1):283-95 18435916 - Biochem Biophys Res Commun. 2008 Jun 27;371(2):283-8 16638023 - J Neurochem. 2006 Jun;97(5):1232-42 19269040 - J Neuroimmunol. 2009 May 29;210(1-2):3-12 16092928 - J Neurochem. 2005 Nov;95(4):919-29 19908286 - J Neurosci Res. 2010 Apr;88(5):1113-23 9570146 - Int J Biochem Cell Biol. 1997 Dec;29(12):1525-39 12006103 - Biochem J. 2002 Aug 1;365(Pt 3):561-75 C Xia (457_CR44) 1997; 29 X Gao (457_CR58) 2011; 76 OS Kim (457_CR5) 2002; 277 H Katsuki (457_CR53) 2006; 97 AY Shih (457_CR12) 2003; 23 C Nerlov (457_CR43) 2008; 20 J Saura (457_CR32) 2003; 85 O Meir (457_CR42) 2010; 5 B Kaltschmidt (457_CR3) 2005; 1745 H Chen (457_CR57) 2005; 58 V Ossipow (457_CR13) 1993; 90 D Giulian (457_CR29) 1986; 6 YW Liu (457_CR35) 2003; 171 K Perez-Capote (457_CR25) 2006; 410 H Li (457_CR51) 2008; 283 GT Liberatore (457_CR55) 1999; 5 D Kwon (457_CR4) 2004; 45 R Kapadia (457_CR26) 2006; 98 W Zhang (457_CR7) 2006; 174 N Gresa-Arribas (457_CR31) 2010; 115 IH Cho (457_CR2) 2008; 131 E Sterneck (457_CR60) 1998; 70 CJ Lowenstein (457_CR19) 1993; 90 KJ Livak (457_CR33) 2001; 25 DP Ramji (457_CR16) 2002; 365 UK Hanisch (457_CR52) 2007; 10 MP Mount (457_CR56) 2007; 27 M Cortes-Canteli (457_CR27) 2008; 121 C Schwartz (457_CR50) 2003; 22 JE Merrill (457_CR48) 1993; 151 SA Friedle (457_CR8) 2011; 59 J Saura (457_CR38) 2005; 95 X Wang (457_CR6) 2008; 371 C Iadecola (457_CR9) 1999; 189 I Screpanti (457_CR28) 1995; 14 JM Lee (457_CR11) 2005; 19 BA in't Veld (457_CR59) 2001; 22 B Gorgoni (457_CR47) 2002; 168 V Poli (457_CR17) 1998; 273 M Caivano (457_CR18) 2001; 276 J Saura (457_CR30) 2003; 44 K Schroder (457_CR41) 2006; 211 CK Glass (457_CR36) 2010; 140 V Ramberg (457_CR46) 2011; 8 LE Greenbaum (457_CR15) 1998; 102 A Michelucci (457_CR1) 2009; 210 MN Bradley (457_CR21) 2003; 23 J Saura (457_CR39) 2007; 4 E Sterneck (457_CR40) 1997; 11 AL Welm (457_CR14) 1999; 19 PD Drew (457_CR10) 2006; 49 ST Reddy (457_CR20) 2000; 275 JR Cardinaux (457_CR22) 2000; 29 A Ejarque-Ortiz (457_CR45) 2010; 88 C Sola (457_CR37) 2002; 16 SP Buira (457_CR34) 2010; 115 A Ejarque-Ortiz (457_CR24) 2007; 55 J Chen (457_CR49) 2010; 107 Z Xie (457_CR54) 2002; 22 JR Cardinaux (457_CR23) 1996; 16 |
References_xml | – volume: 10 start-page: 1387 year: 2007 ident: 457_CR52 publication-title: Nat Neurosci doi: 10.1038/nn1997 contributor: fullname: UK Hanisch – volume: 8 start-page: 34 year: 2011 ident: 457_CR46 publication-title: J Neuroinflammation doi: 10.1186/1742-2094-8-34 contributor: fullname: V Ramberg – volume: 76 start-page: 863 year: 2011 ident: 457_CR58 publication-title: Neurology doi: 10.1212/WNL.0b013e31820f2d79 contributor: fullname: X Gao – volume: 276 start-page: 48693 year: 2001 ident: 457_CR18 publication-title: J Biol Chem doi: 10.1074/jbc.M108282200 contributor: fullname: M Caivano – volume: 6 start-page: 2163 year: 1986 ident: 457_CR29 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.06-08-02163.1986 contributor: fullname: D Giulian – volume: 97 start-page: 1232 year: 2006 ident: 457_CR53 publication-title: J Neurochem doi: 10.1111/j.1471-4159.2006.03752.x contributor: fullname: H Katsuki – volume: 98 start-page: 1718 year: 2006 ident: 457_CR26 publication-title: J Neurochem doi: 10.1111/j.1471-4159.2006.04056.x contributor: fullname: R Kapadia – volume: 23 start-page: 3394 year: 2003 ident: 457_CR12 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.23-08-03394.2003 contributor: fullname: AY Shih – volume: 45 start-page: 287 year: 2004 ident: 457_CR4 publication-title: Glia doi: 10.1002/glia.10331 contributor: fullname: D Kwon – volume: 16 start-page: 919 year: 1996 ident: 457_CR23 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.16-03-00919.1996 contributor: fullname: JR Cardinaux – volume: 4 start-page: 26 year: 2007 ident: 457_CR39 publication-title: J Neuroinflammation doi: 10.1186/1742-2094-4-26 contributor: fullname: J Saura – volume: 174 start-page: 63 year: 2006 ident: 457_CR7 publication-title: J Neuroimmunol doi: 10.1016/j.jneuroim.2006.01.014 contributor: fullname: W Zhang – volume: 49 start-page: 183 year: 2006 ident: 457_CR10 publication-title: Neurochem Int doi: 10.1016/j.neuint.2006.04.003 contributor: fullname: PD Drew – volume: 90 start-page: 9730 year: 1993 ident: 457_CR19 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.90.20.9730 contributor: fullname: CJ Lowenstein – volume: 410 start-page: 25 year: 2006 ident: 457_CR25 publication-title: Neurosci Lett doi: 10.1016/j.neulet.2006.09.078 contributor: fullname: K Perez-Capote – volume: 25 start-page: 402 year: 2001 ident: 457_CR33 publication-title: Methods doi: 10.1006/meth.2001.1262 contributor: fullname: KJ Livak – volume: 189 start-page: 719 year: 1999 ident: 457_CR9 publication-title: J Exp Med doi: 10.1084/jem.189.4.719 contributor: fullname: C Iadecola – volume: 29 start-page: 91 year: 2000 ident: 457_CR22 publication-title: Glia doi: 10.1002/(SICI)1098-1136(20000101)29:1<91::AID-GLIA9>3.0.CO;2-I contributor: fullname: JR Cardinaux – volume: 11 start-page: 2153 year: 1997 ident: 457_CR40 publication-title: Genes Dev doi: 10.1101/gad.11.17.2153 contributor: fullname: E Sterneck – volume: 5 start-page: e9516 year: 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Biol Chem doi: 10.1074/jbc.M203885200 contributor: fullname: OS Kim – volume: 55 start-page: 178 year: 2007 ident: 457_CR24 publication-title: Glia doi: 10.1002/glia.20446 contributor: fullname: A Ejarque-Ortiz – volume: 5 start-page: 1403 year: 1999 ident: 457_CR55 publication-title: Nat Med doi: 10.1038/70978 contributor: fullname: GT Liberatore – volume: 85 start-page: 1455 year: 2003 ident: 457_CR32 publication-title: J Neurochem doi: 10.1046/j.1471-4159.2003.01788.x contributor: fullname: J Saura – volume: 102 start-page: 996 year: 1998 ident: 457_CR15 publication-title: J Clin Invest doi: 10.1172/JCI3135 contributor: fullname: LE Greenbaum – volume: 19 start-page: 1061 year: 2005 ident: 457_CR11 publication-title: FASEB J doi: 10.1096/fj.04-2591hyp contributor: fullname: JM Lee – volume: 211 start-page: 511 year: 2006 ident: 457_CR41 publication-title: Immunobiology doi: 10.1016/j.imbio.2006.05.007 contributor: fullname: K Schroder – volume: 95 start-page: 919 year: 2005 ident: 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Snippet | Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial activation or... Abstract Background Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial... BACKGROUND: Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial activation or... Background. Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial activation or... Abstract Background Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial... |
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SubjectTerms | Animals Astrocytes - cytology Astrocytes - drug effects Astrocytes - physiology CCAAT-Enhancer-Binding Protein-beta - genetics CCAAT-Enhancer-Binding Protein-beta - metabolism Cells, Cultured Coculture Techniques Cytokines - genetics Cytokines - metabolism Expressió gènica Female Gene Expression Inflamació Inflammation Inflammation - genetics Inflammation - metabolism Interferon-gamma - pharmacology Lipopolysaccharides - pharmacology Mice Mice, Inbred C57BL Mice, Knockout Microglia - cytology Microglia - drug effects Microglia - physiology Neurons - cytology Neurons - physiology Neurotoxicologia Neurotoxicology Nitric Oxide - metabolism Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type II - metabolism Pregnancy |
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Title | Pro-inflammatory gene expression and neurotoxic effects of activated microglia are attenuated by absence of CCAAT/enhancer binding protein β |
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