Fasudil attenuates glial cell-mediated neuroinflammation via ERK1/2 and AKT signaling pathways after optic nerve crush
To investigate the functional role of fasudil in optic nerve crush (ONC), and further explore its possible molecular mechanism. After ONC injury, the rats were injected intraperitoneally either with fasudil or normal saline once a day until euthanized. RGCs survival was assessed by retrograde labeli...
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| Veröffentlicht in: | Molecular biology reports 2020-11, Vol.47 (11), p.8963-8973 |
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| creator | Huang, Wei Lan, Qianqian Jiang, Li Yan, Wenya Tang, Fen Shen, Chaolan Huang, Hui Zhong, Haibin Lv, Jian Zeng, Siming Li, Min Mo, Zhongxiang Hu, Bing Liang, Ning Chen, Qi Zhang, Mingyuan Xu, Fan Cui, Ling |
| description | To investigate the functional role of fasudil in optic nerve crush (ONC), and further explore its possible molecular mechanism. After ONC injury, the rats were injected intraperitoneally either with fasudil or normal saline once a day until euthanized. RGCs survival was assessed by retrograde labeling with FluoroGold. Retinal glial cells activation and population changes (GFAP, iba-1) were measured by immunofluorescence. The expressions of cleaved caspase 3 and 9, p-ERK1/2 and p-AKT were detected by western blot. The levels of the pro-inflammatory cytokines were determined using real-time polymerase chain reaction. Fasudil treatment inhibited RGCs apoptosis and reduced RGCs loss demonstrated by the decreased apoptosis-associated proteins expression and the increased fluorogold labeling of RGCs after ONC, respectively. In addition, the ONC + fasudil group compared had a significantly lower expression of GFAP and iba1 compared with the ONC group. The levels of pro-inflammatory cytokines were significantly reduced in the ONC + fasudil group than in the ONC group. Furthermore, the phosphorylation levels of ERK1/2 and AKT (p-ERK1/2 and p-AKT) were obviously elevated by the fasudil treatment. Our study demonstrated that fasudil attenuated glial cell-mediated neuroinflammation by up-regulating the ERK1/2 and AKT signaling pathways in rats ONC models. We conclude that fasudil may be a novel treatment for traumatic optic neuropathy. |
| doi_str_mv | 10.1007/s11033-020-05953-y |
| format | Article |
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After ONC injury, the rats were injected intraperitoneally either with fasudil or normal saline once a day until euthanized. RGCs survival was assessed by retrograde labeling with FluoroGold. Retinal glial cells activation and population changes (GFAP, iba-1) were measured by immunofluorescence. The expressions of cleaved caspase 3 and 9, p-ERK1/2 and p-AKT were detected by western blot. The levels of the pro-inflammatory cytokines were determined using real-time polymerase chain reaction. Fasudil treatment inhibited RGCs apoptosis and reduced RGCs loss demonstrated by the decreased apoptosis-associated proteins expression and the increased fluorogold labeling of RGCs after ONC, respectively. In addition, the ONC + fasudil group compared had a significantly lower expression of GFAP and iba1 compared with the ONC group. The levels of pro-inflammatory cytokines were significantly reduced in the ONC + fasudil group than in the ONC group. Furthermore, the phosphorylation levels of ERK1/2 and AKT (p-ERK1/2 and p-AKT) were obviously elevated by the fasudil treatment. Our study demonstrated that fasudil attenuated glial cell-mediated neuroinflammation by up-regulating the ERK1/2 and AKT signaling pathways in rats ONC models. We conclude that fasudil may be a novel treatment for traumatic optic neuropathy.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-020-05953-y</identifier><identifier>PMID: 33161529</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>AKT protein ; Animal Anatomy ; Animal Biochemistry ; Animal models ; Apoptosis ; Biomedical and Life Sciences ; Caspase-3 ; Cell activation ; Cytokines ; Extracellular signal-regulated kinase ; Glial cells ; Glial fibrillary acidic protein ; Histology ; Immunofluorescence ; Inflammation ; Life Sciences ; Morphology ; Neuronal-glial interactions ; Optic nerve ; Optic neuropathy ; Original Article ; Phosphorylation ; Polymerase chain reaction ; Population changes ; Signal transduction</subject><ispartof>Molecular biology reports, 2020-11, Vol.47 (11), p.8963-8973</ispartof><rights>Springer Nature B.V. 2020</rights><rights>Springer Nature B.V. 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-c8ac74a80f91bfee5fe0ecaca1ca9e8e5334bfdb72d22afbf39e3a9556038363</citedby><cites>FETCH-LOGICAL-c375t-c8ac74a80f91bfee5fe0ecaca1ca9e8e5334bfdb72d22afbf39e3a9556038363</cites><orcidid>0000-0002-1504-2356</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11033-020-05953-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-020-05953-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33161529$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Wei</creatorcontrib><creatorcontrib>Lan, Qianqian</creatorcontrib><creatorcontrib>Jiang, Li</creatorcontrib><creatorcontrib>Yan, Wenya</creatorcontrib><creatorcontrib>Tang, Fen</creatorcontrib><creatorcontrib>Shen, Chaolan</creatorcontrib><creatorcontrib>Huang, Hui</creatorcontrib><creatorcontrib>Zhong, Haibin</creatorcontrib><creatorcontrib>Lv, Jian</creatorcontrib><creatorcontrib>Zeng, Siming</creatorcontrib><creatorcontrib>Li, Min</creatorcontrib><creatorcontrib>Mo, Zhongxiang</creatorcontrib><creatorcontrib>Hu, Bing</creatorcontrib><creatorcontrib>Liang, Ning</creatorcontrib><creatorcontrib>Chen, Qi</creatorcontrib><creatorcontrib>Zhang, Mingyuan</creatorcontrib><creatorcontrib>Xu, Fan</creatorcontrib><creatorcontrib>Cui, Ling</creatorcontrib><title>Fasudil attenuates glial cell-mediated neuroinflammation via ERK1/2 and AKT signaling pathways after optic nerve crush</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>To investigate the functional role of fasudil in optic nerve crush (ONC), and further explore its possible molecular mechanism. After ONC injury, the rats were injected intraperitoneally either with fasudil or normal saline once a day until euthanized. RGCs survival was assessed by retrograde labeling with FluoroGold. Retinal glial cells activation and population changes (GFAP, iba-1) were measured by immunofluorescence. The expressions of cleaved caspase 3 and 9, p-ERK1/2 and p-AKT were detected by western blot. The levels of the pro-inflammatory cytokines were determined using real-time polymerase chain reaction. Fasudil treatment inhibited RGCs apoptosis and reduced RGCs loss demonstrated by the decreased apoptosis-associated proteins expression and the increased fluorogold labeling of RGCs after ONC, respectively. In addition, the ONC + fasudil group compared had a significantly lower expression of GFAP and iba1 compared with the ONC group. The levels of pro-inflammatory cytokines were significantly reduced in the ONC + fasudil group than in the ONC group. Furthermore, the phosphorylation levels of ERK1/2 and AKT (p-ERK1/2 and p-AKT) were obviously elevated by the fasudil treatment. Our study demonstrated that fasudil attenuated glial cell-mediated neuroinflammation by up-regulating the ERK1/2 and AKT signaling pathways in rats ONC models. We conclude that fasudil may be a novel treatment for traumatic optic neuropathy.</description><subject>AKT protein</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Animal models</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Caspase-3</subject><subject>Cell activation</subject><subject>Cytokines</subject><subject>Extracellular signal-regulated kinase</subject><subject>Glial cells</subject><subject>Glial fibrillary acidic protein</subject><subject>Histology</subject><subject>Immunofluorescence</subject><subject>Inflammation</subject><subject>Life Sciences</subject><subject>Morphology</subject><subject>Neuronal-glial interactions</subject><subject>Optic nerve</subject><subject>Optic neuropathy</subject><subject>Original Article</subject><subject>Phosphorylation</subject><subject>Polymerase chain reaction</subject><subject>Population changes</subject><subject>Signal 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protein</topic><topic>Histology</topic><topic>Immunofluorescence</topic><topic>Inflammation</topic><topic>Life Sciences</topic><topic>Morphology</topic><topic>Neuronal-glial interactions</topic><topic>Optic nerve</topic><topic>Optic neuropathy</topic><topic>Original Article</topic><topic>Phosphorylation</topic><topic>Polymerase chain reaction</topic><topic>Population changes</topic><topic>Signal transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Wei</creatorcontrib><creatorcontrib>Lan, Qianqian</creatorcontrib><creatorcontrib>Jiang, Li</creatorcontrib><creatorcontrib>Yan, Wenya</creatorcontrib><creatorcontrib>Tang, Fen</creatorcontrib><creatorcontrib>Shen, Chaolan</creatorcontrib><creatorcontrib>Huang, Hui</creatorcontrib><creatorcontrib>Zhong, Haibin</creatorcontrib><creatorcontrib>Lv, Jian</creatorcontrib><creatorcontrib>Zeng, Siming</creatorcontrib><creatorcontrib>Li, Min</creatorcontrib><creatorcontrib>Mo, 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Jian</au><au>Zeng, Siming</au><au>Li, Min</au><au>Mo, Zhongxiang</au><au>Hu, Bing</au><au>Liang, Ning</au><au>Chen, Qi</au><au>Zhang, Mingyuan</au><au>Xu, Fan</au><au>Cui, Ling</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fasudil attenuates glial cell-mediated neuroinflammation via ERK1/2 and AKT signaling pathways after optic nerve crush</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2020-11-01</date><risdate>2020</risdate><volume>47</volume><issue>11</issue><spage>8963</spage><epage>8973</epage><pages>8963-8973</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>To investigate the functional role of fasudil in optic nerve crush (ONC), and further explore its possible molecular mechanism. After ONC injury, the rats were injected intraperitoneally either with fasudil or normal saline once a day until euthanized. RGCs survival was assessed by retrograde labeling with FluoroGold. Retinal glial cells activation and population changes (GFAP, iba-1) were measured by immunofluorescence. The expressions of cleaved caspase 3 and 9, p-ERK1/2 and p-AKT were detected by western blot. The levels of the pro-inflammatory cytokines were determined using real-time polymerase chain reaction. Fasudil treatment inhibited RGCs apoptosis and reduced RGCs loss demonstrated by the decreased apoptosis-associated proteins expression and the increased fluorogold labeling of RGCs after ONC, respectively. In addition, the ONC + fasudil group compared had a significantly lower expression of GFAP and iba1 compared with the ONC group. The levels of pro-inflammatory cytokines were significantly reduced in the ONC + fasudil group than in the ONC group. Furthermore, the phosphorylation levels of ERK1/2 and AKT (p-ERK1/2 and p-AKT) were obviously elevated by the fasudil treatment. Our study demonstrated that fasudil attenuated glial cell-mediated neuroinflammation by up-regulating the ERK1/2 and AKT signaling pathways in rats ONC models. We conclude that fasudil may be a novel treatment for traumatic optic neuropathy.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>33161529</pmid><doi>10.1007/s11033-020-05953-y</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-1504-2356</orcidid></addata></record> |
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| subjects | AKT protein Animal Anatomy Animal Biochemistry Animal models Apoptosis Biomedical and Life Sciences Caspase-3 Cell activation Cytokines Extracellular signal-regulated kinase Glial cells Glial fibrillary acidic protein Histology Immunofluorescence Inflammation Life Sciences Morphology Neuronal-glial interactions Optic nerve Optic neuropathy Original Article Phosphorylation Polymerase chain reaction Population changes Signal transduction |
| title | Fasudil attenuates glial cell-mediated neuroinflammation via ERK1/2 and AKT signaling pathways after optic nerve crush |
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