$ H_{2} $S Regulates the Phenotypic Transformation of Astrocytes Following Cerebral Ischemia/Reperfusion via Inhibiting the RhoA/ROCK Pathway
Abstract The role of hydrogen sulfide ($ H_{2} $S) on the phenotypic change of astrocytes following cerebral ischemia/reperfusion (I/R) in mice was investigated in present study. We tested the expression of glial fibrillary acidic protein (GFAP), A2 phenotype marker S100a10, and A1 phenotype marker...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Ding, Yanyu [verfasserIn] Fang, Fang [verfasserIn] Liu, Xiaolong [verfasserIn] Sheng, Shuyan [verfasserIn] Li, Xueyan [verfasserIn] Yin, Xiaojiao [verfasserIn] Chen, Zhiwu [verfasserIn] Wen, Jiyue [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2023 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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| Übergeordnetes Werk: |
Enthalten in: Molecular neurobiology - Springer US, 1987, 61(2023), 6 vom: 18. Nov., Seite 3179-3197 |
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| Übergeordnetes Werk: |
volume:61 ; year:2023 ; number:6 ; day:18 ; month:11 ; pages:3179-3197 |
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| DOI / URN: |
10.1007/s12035-023-03797-8 |
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| Katalog-ID: |
SPR055810640 |
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| 520 | |a Abstract The role of hydrogen sulfide ($ H_{2} $S) on the phenotypic change of astrocytes following cerebral ischemia/reperfusion (I/R) in mice was investigated in present study. We tested the expression of glial fibrillary acidic protein (GFAP), A2 phenotype marker S100a10, and A1 phenotype marker C3 protein and assessed the change of BrdU/GFAP-positive cells, GFAP/C3-positive cells, and GFAP/S100a10-positive cells in mice hippocampal tissues to evaluate the change of astrocyte phenotypes following cerebral I/R. The role of $ H_{2} $S on the phenotypic change of astrocytes following cerebral I/R in mice was investigated by using $ H_{2} $S synthase cystathionine-γ-lyase (CSE) knockout mice (KO). The results revealed that cerebral I/R injury promoted the astrocytes proliferation of both A1 and A2 phenotypes, which were more significant in mice of $ H_{2} $S synthase CSE KO than in mice of wild type (WT). Interestingly, supplement with $ H_{2} $S could inhibit the A1 phenotype proliferation but promote the proliferation of A2 phenotype, suggesting that $ H_{2} $S could regulate the transformation of astrocytes to A2 phenotype following cerebral I/R, which is beneficial for neuronal recovery. Besides, we found that $ H_{2} $S-mediated change of astrocyte phenotype is related to inhibiting the RhoA/ROCK pathway. Furthermore, both $ H_{2} $S and ROCK inhibitor could ameliorate the brain injury of mice at 9 days after cerebral I/R. In conclusion, $ H_{2} $S regulates the phenotypic transformation of astrocytes to A2 phenotype following the cerebral I/R via inhibiting RhoA/ROCK pathway and then exerts the neuroprotective effect against the subacute brain injury. | ||
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10.1007/s12035-023-03797-8 doi (DE-627)SPR055810640 (SPR)s12035-023-03797-8-e DE-627 ger DE-627 rakwb eng 610 570 VZ 44.90 bkl Ding, Yanyu verfasserin aut $ H_{2} $S Regulates the Phenotypic Transformation of Astrocytes Following Cerebral Ischemia/Reperfusion via Inhibiting the RhoA/ROCK Pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The role of hydrogen sulfide ($ H_{2} $S) on the phenotypic change of astrocytes following cerebral ischemia/reperfusion (I/R) in mice was investigated in present study. We tested the expression of glial fibrillary acidic protein (GFAP), A2 phenotype marker S100a10, and A1 phenotype marker C3 protein and assessed the change of BrdU/GFAP-positive cells, GFAP/C3-positive cells, and GFAP/S100a10-positive cells in mice hippocampal tissues to evaluate the change of astrocyte phenotypes following cerebral I/R. The role of $ H_{2} $S on the phenotypic change of astrocytes following cerebral I/R in mice was investigated by using $ H_{2} $S synthase cystathionine-γ-lyase (CSE) knockout mice (KO). The results revealed that cerebral I/R injury promoted the astrocytes proliferation of both A1 and A2 phenotypes, which were more significant in mice of $ H_{2} $S synthase CSE KO than in mice of wild type (WT). Interestingly, supplement with $ H_{2} $S could inhibit the A1 phenotype proliferation but promote the proliferation of A2 phenotype, suggesting that $ H_{2} $S could regulate the transformation of astrocytes to A2 phenotype following cerebral I/R, which is beneficial for neuronal recovery. Besides, we found that $ H_{2} $S-mediated change of astrocyte phenotype is related to inhibiting the RhoA/ROCK pathway. Furthermore, both $ H_{2} $S and ROCK inhibitor could ameliorate the brain injury of mice at 9 days after cerebral I/R. In conclusion, $ H_{2} $S regulates the phenotypic transformation of astrocytes to A2 phenotype following the cerebral I/R via inhibiting RhoA/ROCK pathway and then exerts the neuroprotective effect against the subacute brain injury. H (dpeaa)DE-He213 S (dpeaa)DE-He213 Cerebral I/R (dpeaa)DE-He213 Astrocytes (dpeaa)DE-He213 A2 phenotype (dpeaa)DE-He213 RhoA/ROCK pathway (dpeaa)DE-He213 Fang, Fang verfasserin aut Liu, Xiaolong verfasserin aut Sheng, Shuyan verfasserin aut Li, Xueyan verfasserin aut Yin, Xiaojiao verfasserin aut Chen, Zhiwu verfasserin aut Wen, Jiyue verfasserin (orcid)0000-0002-7602-1727 aut Enthalten in Molecular neurobiology Springer US, 1987 61(2023), 6 vom: 18. Nov., Seite 3179-3197 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:61 year:2023 number:6 day:18 month:11 pages:3179-3197 https://dx.doi.org/10.1007/s12035-023-03797-8 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 VZ AR 61 2023 6 18 11 3179-3197 |
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10.1007/s12035-023-03797-8 doi (DE-627)SPR055810640 (SPR)s12035-023-03797-8-e DE-627 ger DE-627 rakwb eng 610 570 VZ 44.90 bkl Ding, Yanyu verfasserin aut $ H_{2} $S Regulates the Phenotypic Transformation of Astrocytes Following Cerebral Ischemia/Reperfusion via Inhibiting the RhoA/ROCK Pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The role of hydrogen sulfide ($ H_{2} $S) on the phenotypic change of astrocytes following cerebral ischemia/reperfusion (I/R) in mice was investigated in present study. We tested the expression of glial fibrillary acidic protein (GFAP), A2 phenotype marker S100a10, and A1 phenotype marker C3 protein and assessed the change of BrdU/GFAP-positive cells, GFAP/C3-positive cells, and GFAP/S100a10-positive cells in mice hippocampal tissues to evaluate the change of astrocyte phenotypes following cerebral I/R. The role of $ H_{2} $S on the phenotypic change of astrocytes following cerebral I/R in mice was investigated by using $ H_{2} $S synthase cystathionine-γ-lyase (CSE) knockout mice (KO). The results revealed that cerebral I/R injury promoted the astrocytes proliferation of both A1 and A2 phenotypes, which were more significant in mice of $ H_{2} $S synthase CSE KO than in mice of wild type (WT). Interestingly, supplement with $ H_{2} $S could inhibit the A1 phenotype proliferation but promote the proliferation of A2 phenotype, suggesting that $ H_{2} $S could regulate the transformation of astrocytes to A2 phenotype following cerebral I/R, which is beneficial for neuronal recovery. Besides, we found that $ H_{2} $S-mediated change of astrocyte phenotype is related to inhibiting the RhoA/ROCK pathway. Furthermore, both $ H_{2} $S and ROCK inhibitor could ameliorate the brain injury of mice at 9 days after cerebral I/R. In conclusion, $ H_{2} $S regulates the phenotypic transformation of astrocytes to A2 phenotype following the cerebral I/R via inhibiting RhoA/ROCK pathway and then exerts the neuroprotective effect against the subacute brain injury. H (dpeaa)DE-He213 S (dpeaa)DE-He213 Cerebral I/R (dpeaa)DE-He213 Astrocytes (dpeaa)DE-He213 A2 phenotype (dpeaa)DE-He213 RhoA/ROCK pathway (dpeaa)DE-He213 Fang, Fang verfasserin aut Liu, Xiaolong verfasserin aut Sheng, Shuyan verfasserin aut Li, Xueyan verfasserin aut Yin, Xiaojiao verfasserin aut Chen, Zhiwu verfasserin aut Wen, Jiyue verfasserin (orcid)0000-0002-7602-1727 aut Enthalten in Molecular neurobiology Springer US, 1987 61(2023), 6 vom: 18. Nov., Seite 3179-3197 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:61 year:2023 number:6 day:18 month:11 pages:3179-3197 https://dx.doi.org/10.1007/s12035-023-03797-8 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 VZ AR 61 2023 6 18 11 3179-3197 |
| allfields_unstemmed |
10.1007/s12035-023-03797-8 doi (DE-627)SPR055810640 (SPR)s12035-023-03797-8-e DE-627 ger DE-627 rakwb eng 610 570 VZ 44.90 bkl Ding, Yanyu verfasserin aut $ H_{2} $S Regulates the Phenotypic Transformation of Astrocytes Following Cerebral Ischemia/Reperfusion via Inhibiting the RhoA/ROCK Pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The role of hydrogen sulfide ($ H_{2} $S) on the phenotypic change of astrocytes following cerebral ischemia/reperfusion (I/R) in mice was investigated in present study. We tested the expression of glial fibrillary acidic protein (GFAP), A2 phenotype marker S100a10, and A1 phenotype marker C3 protein and assessed the change of BrdU/GFAP-positive cells, GFAP/C3-positive cells, and GFAP/S100a10-positive cells in mice hippocampal tissues to evaluate the change of astrocyte phenotypes following cerebral I/R. The role of $ H_{2} $S on the phenotypic change of astrocytes following cerebral I/R in mice was investigated by using $ H_{2} $S synthase cystathionine-γ-lyase (CSE) knockout mice (KO). The results revealed that cerebral I/R injury promoted the astrocytes proliferation of both A1 and A2 phenotypes, which were more significant in mice of $ H_{2} $S synthase CSE KO than in mice of wild type (WT). Interestingly, supplement with $ H_{2} $S could inhibit the A1 phenotype proliferation but promote the proliferation of A2 phenotype, suggesting that $ H_{2} $S could regulate the transformation of astrocytes to A2 phenotype following cerebral I/R, which is beneficial for neuronal recovery. Besides, we found that $ H_{2} $S-mediated change of astrocyte phenotype is related to inhibiting the RhoA/ROCK pathway. Furthermore, both $ H_{2} $S and ROCK inhibitor could ameliorate the brain injury of mice at 9 days after cerebral I/R. In conclusion, $ H_{2} $S regulates the phenotypic transformation of astrocytes to A2 phenotype following the cerebral I/R via inhibiting RhoA/ROCK pathway and then exerts the neuroprotective effect against the subacute brain injury. H (dpeaa)DE-He213 S (dpeaa)DE-He213 Cerebral I/R (dpeaa)DE-He213 Astrocytes (dpeaa)DE-He213 A2 phenotype (dpeaa)DE-He213 RhoA/ROCK pathway (dpeaa)DE-He213 Fang, Fang verfasserin aut Liu, Xiaolong verfasserin aut Sheng, Shuyan verfasserin aut Li, Xueyan verfasserin aut Yin, Xiaojiao verfasserin aut Chen, Zhiwu verfasserin aut Wen, Jiyue verfasserin (orcid)0000-0002-7602-1727 aut Enthalten in Molecular neurobiology Springer US, 1987 61(2023), 6 vom: 18. Nov., Seite 3179-3197 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:61 year:2023 number:6 day:18 month:11 pages:3179-3197 https://dx.doi.org/10.1007/s12035-023-03797-8 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 VZ AR 61 2023 6 18 11 3179-3197 |
| allfieldsGer |
10.1007/s12035-023-03797-8 doi (DE-627)SPR055810640 (SPR)s12035-023-03797-8-e DE-627 ger DE-627 rakwb eng 610 570 VZ 44.90 bkl Ding, Yanyu verfasserin aut $ H_{2} $S Regulates the Phenotypic Transformation of Astrocytes Following Cerebral Ischemia/Reperfusion via Inhibiting the RhoA/ROCK Pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The role of hydrogen sulfide ($ H_{2} $S) on the phenotypic change of astrocytes following cerebral ischemia/reperfusion (I/R) in mice was investigated in present study. We tested the expression of glial fibrillary acidic protein (GFAP), A2 phenotype marker S100a10, and A1 phenotype marker C3 protein and assessed the change of BrdU/GFAP-positive cells, GFAP/C3-positive cells, and GFAP/S100a10-positive cells in mice hippocampal tissues to evaluate the change of astrocyte phenotypes following cerebral I/R. The role of $ H_{2} $S on the phenotypic change of astrocytes following cerebral I/R in mice was investigated by using $ H_{2} $S synthase cystathionine-γ-lyase (CSE) knockout mice (KO). The results revealed that cerebral I/R injury promoted the astrocytes proliferation of both A1 and A2 phenotypes, which were more significant in mice of $ H_{2} $S synthase CSE KO than in mice of wild type (WT). Interestingly, supplement with $ H_{2} $S could inhibit the A1 phenotype proliferation but promote the proliferation of A2 phenotype, suggesting that $ H_{2} $S could regulate the transformation of astrocytes to A2 phenotype following cerebral I/R, which is beneficial for neuronal recovery. Besides, we found that $ H_{2} $S-mediated change of astrocyte phenotype is related to inhibiting the RhoA/ROCK pathway. Furthermore, both $ H_{2} $S and ROCK inhibitor could ameliorate the brain injury of mice at 9 days after cerebral I/R. In conclusion, $ H_{2} $S regulates the phenotypic transformation of astrocytes to A2 phenotype following the cerebral I/R via inhibiting RhoA/ROCK pathway and then exerts the neuroprotective effect against the subacute brain injury. H (dpeaa)DE-He213 S (dpeaa)DE-He213 Cerebral I/R (dpeaa)DE-He213 Astrocytes (dpeaa)DE-He213 A2 phenotype (dpeaa)DE-He213 RhoA/ROCK pathway (dpeaa)DE-He213 Fang, Fang verfasserin aut Liu, Xiaolong verfasserin aut Sheng, Shuyan verfasserin aut Li, Xueyan verfasserin aut Yin, Xiaojiao verfasserin aut Chen, Zhiwu verfasserin aut Wen, Jiyue verfasserin (orcid)0000-0002-7602-1727 aut Enthalten in Molecular neurobiology Springer US, 1987 61(2023), 6 vom: 18. Nov., Seite 3179-3197 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:61 year:2023 number:6 day:18 month:11 pages:3179-3197 https://dx.doi.org/10.1007/s12035-023-03797-8 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 VZ AR 61 2023 6 18 11 3179-3197 |
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10.1007/s12035-023-03797-8 doi (DE-627)SPR055810640 (SPR)s12035-023-03797-8-e DE-627 ger DE-627 rakwb eng 610 570 VZ 44.90 bkl Ding, Yanyu verfasserin aut $ H_{2} $S Regulates the Phenotypic Transformation of Astrocytes Following Cerebral Ischemia/Reperfusion via Inhibiting the RhoA/ROCK Pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The role of hydrogen sulfide ($ H_{2} $S) on the phenotypic change of astrocytes following cerebral ischemia/reperfusion (I/R) in mice was investigated in present study. We tested the expression of glial fibrillary acidic protein (GFAP), A2 phenotype marker S100a10, and A1 phenotype marker C3 protein and assessed the change of BrdU/GFAP-positive cells, GFAP/C3-positive cells, and GFAP/S100a10-positive cells in mice hippocampal tissues to evaluate the change of astrocyte phenotypes following cerebral I/R. The role of $ H_{2} $S on the phenotypic change of astrocytes following cerebral I/R in mice was investigated by using $ H_{2} $S synthase cystathionine-γ-lyase (CSE) knockout mice (KO). The results revealed that cerebral I/R injury promoted the astrocytes proliferation of both A1 and A2 phenotypes, which were more significant in mice of $ H_{2} $S synthase CSE KO than in mice of wild type (WT). Interestingly, supplement with $ H_{2} $S could inhibit the A1 phenotype proliferation but promote the proliferation of A2 phenotype, suggesting that $ H_{2} $S could regulate the transformation of astrocytes to A2 phenotype following cerebral I/R, which is beneficial for neuronal recovery. Besides, we found that $ H_{2} $S-mediated change of astrocyte phenotype is related to inhibiting the RhoA/ROCK pathway. Furthermore, both $ H_{2} $S and ROCK inhibitor could ameliorate the brain injury of mice at 9 days after cerebral I/R. In conclusion, $ H_{2} $S regulates the phenotypic transformation of astrocytes to A2 phenotype following the cerebral I/R via inhibiting RhoA/ROCK pathway and then exerts the neuroprotective effect against the subacute brain injury. H (dpeaa)DE-He213 S (dpeaa)DE-He213 Cerebral I/R (dpeaa)DE-He213 Astrocytes (dpeaa)DE-He213 A2 phenotype (dpeaa)DE-He213 RhoA/ROCK pathway (dpeaa)DE-He213 Fang, Fang verfasserin aut Liu, Xiaolong verfasserin aut Sheng, Shuyan verfasserin aut Li, Xueyan verfasserin aut Yin, Xiaojiao verfasserin aut Chen, Zhiwu verfasserin aut Wen, Jiyue verfasserin (orcid)0000-0002-7602-1727 aut Enthalten in Molecular neurobiology Springer US, 1987 61(2023), 6 vom: 18. Nov., Seite 3179-3197 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:61 year:2023 number:6 day:18 month:11 pages:3179-3197 https://dx.doi.org/10.1007/s12035-023-03797-8 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 VZ AR 61 2023 6 18 11 3179-3197 |
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Enthalten in Molecular neurobiology 61(2023), 6 vom: 18. Nov., Seite 3179-3197 volume:61 year:2023 number:6 day:18 month:11 pages:3179-3197 |
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Ding, Yanyu @@aut@@ Fang, Fang @@aut@@ Liu, Xiaolong @@aut@@ Sheng, Shuyan @@aut@@ Li, Xueyan @@aut@@ Yin, Xiaojiao @@aut@@ Chen, Zhiwu @@aut@@ Wen, Jiyue @@aut@@ |
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Ding, Yanyu |
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Ding, Yanyu ddc 610 bkl 44.90 misc H misc S misc Cerebral I/R misc Astrocytes misc A2 phenotype misc RhoA/ROCK pathway $ H_{2} $S Regulates the Phenotypic Transformation of Astrocytes Following Cerebral Ischemia/Reperfusion via Inhibiting the RhoA/ROCK Pathway |
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$ H_{2} $S Regulates the Phenotypic Transformation of Astrocytes Following Cerebral Ischemia/Reperfusion via Inhibiting the RhoA/ROCK Pathway |
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$ H_{2} $S Regulates the Phenotypic Transformation of Astrocytes Following Cerebral Ischemia/Reperfusion via Inhibiting the RhoA/ROCK Pathway |
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Ding, Yanyu Fang, Fang Liu, Xiaolong Sheng, Shuyan Li, Xueyan Yin, Xiaojiao Chen, Zhiwu Wen, Jiyue |
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$ h_{2} $s regulates the phenotypic transformation of astrocytes following cerebral ischemia/reperfusion via inhibiting the rhoa/rock pathway |
| title_auth |
$ H_{2} $S Regulates the Phenotypic Transformation of Astrocytes Following Cerebral Ischemia/Reperfusion via Inhibiting the RhoA/ROCK Pathway |
| abstract |
Abstract The role of hydrogen sulfide ($ H_{2} $S) on the phenotypic change of astrocytes following cerebral ischemia/reperfusion (I/R) in mice was investigated in present study. We tested the expression of glial fibrillary acidic protein (GFAP), A2 phenotype marker S100a10, and A1 phenotype marker C3 protein and assessed the change of BrdU/GFAP-positive cells, GFAP/C3-positive cells, and GFAP/S100a10-positive cells in mice hippocampal tissues to evaluate the change of astrocyte phenotypes following cerebral I/R. The role of $ H_{2} $S on the phenotypic change of astrocytes following cerebral I/R in mice was investigated by using $ H_{2} $S synthase cystathionine-γ-lyase (CSE) knockout mice (KO). The results revealed that cerebral I/R injury promoted the astrocytes proliferation of both A1 and A2 phenotypes, which were more significant in mice of $ H_{2} $S synthase CSE KO than in mice of wild type (WT). Interestingly, supplement with $ H_{2} $S could inhibit the A1 phenotype proliferation but promote the proliferation of A2 phenotype, suggesting that $ H_{2} $S could regulate the transformation of astrocytes to A2 phenotype following cerebral I/R, which is beneficial for neuronal recovery. Besides, we found that $ H_{2} $S-mediated change of astrocyte phenotype is related to inhibiting the RhoA/ROCK pathway. Furthermore, both $ H_{2} $S and ROCK inhibitor could ameliorate the brain injury of mice at 9 days after cerebral I/R. In conclusion, $ H_{2} $S regulates the phenotypic transformation of astrocytes to A2 phenotype following the cerebral I/R via inhibiting RhoA/ROCK pathway and then exerts the neuroprotective effect against the subacute brain injury. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstractGer |
Abstract The role of hydrogen sulfide ($ H_{2} $S) on the phenotypic change of astrocytes following cerebral ischemia/reperfusion (I/R) in mice was investigated in present study. We tested the expression of glial fibrillary acidic protein (GFAP), A2 phenotype marker S100a10, and A1 phenotype marker C3 protein and assessed the change of BrdU/GFAP-positive cells, GFAP/C3-positive cells, and GFAP/S100a10-positive cells in mice hippocampal tissues to evaluate the change of astrocyte phenotypes following cerebral I/R. The role of $ H_{2} $S on the phenotypic change of astrocytes following cerebral I/R in mice was investigated by using $ H_{2} $S synthase cystathionine-γ-lyase (CSE) knockout mice (KO). The results revealed that cerebral I/R injury promoted the astrocytes proliferation of both A1 and A2 phenotypes, which were more significant in mice of $ H_{2} $S synthase CSE KO than in mice of wild type (WT). Interestingly, supplement with $ H_{2} $S could inhibit the A1 phenotype proliferation but promote the proliferation of A2 phenotype, suggesting that $ H_{2} $S could regulate the transformation of astrocytes to A2 phenotype following cerebral I/R, which is beneficial for neuronal recovery. Besides, we found that $ H_{2} $S-mediated change of astrocyte phenotype is related to inhibiting the RhoA/ROCK pathway. Furthermore, both $ H_{2} $S and ROCK inhibitor could ameliorate the brain injury of mice at 9 days after cerebral I/R. In conclusion, $ H_{2} $S regulates the phenotypic transformation of astrocytes to A2 phenotype following the cerebral I/R via inhibiting RhoA/ROCK pathway and then exerts the neuroprotective effect against the subacute brain injury. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstract_unstemmed |
Abstract The role of hydrogen sulfide ($ H_{2} $S) on the phenotypic change of astrocytes following cerebral ischemia/reperfusion (I/R) in mice was investigated in present study. We tested the expression of glial fibrillary acidic protein (GFAP), A2 phenotype marker S100a10, and A1 phenotype marker C3 protein and assessed the change of BrdU/GFAP-positive cells, GFAP/C3-positive cells, and GFAP/S100a10-positive cells in mice hippocampal tissues to evaluate the change of astrocyte phenotypes following cerebral I/R. The role of $ H_{2} $S on the phenotypic change of astrocytes following cerebral I/R in mice was investigated by using $ H_{2} $S synthase cystathionine-γ-lyase (CSE) knockout mice (KO). The results revealed that cerebral I/R injury promoted the astrocytes proliferation of both A1 and A2 phenotypes, which were more significant in mice of $ H_{2} $S synthase CSE KO than in mice of wild type (WT). Interestingly, supplement with $ H_{2} $S could inhibit the A1 phenotype proliferation but promote the proliferation of A2 phenotype, suggesting that $ H_{2} $S could regulate the transformation of astrocytes to A2 phenotype following cerebral I/R, which is beneficial for neuronal recovery. Besides, we found that $ H_{2} $S-mediated change of astrocyte phenotype is related to inhibiting the RhoA/ROCK pathway. Furthermore, both $ H_{2} $S and ROCK inhibitor could ameliorate the brain injury of mice at 9 days after cerebral I/R. In conclusion, $ H_{2} $S regulates the phenotypic transformation of astrocytes to A2 phenotype following the cerebral I/R via inhibiting RhoA/ROCK pathway and then exerts the neuroprotective effect against the subacute brain injury. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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$ H_{2} $S Regulates the Phenotypic Transformation of Astrocytes Following Cerebral Ischemia/Reperfusion via Inhibiting the RhoA/ROCK Pathway |
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https://dx.doi.org/10.1007/s12035-023-03797-8 |
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Fang, Fang Liu, Xiaolong Sheng, Shuyan Li, Xueyan Yin, Xiaojiao Chen, Zhiwu Wen, Jiyue |
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| score |
7.402231 |