Samuel Shao-Min Zhang, Hong Li, Ping Huang, Lucy Xi Lou, Xin-Yuan Fu, Colin J Barnstable
{"title":"视网膜外植体培养中突触神经胶质细胞发育过程中的MAPK信号传导。","authors":"Samuel Shao-Min Zhang, Hong Li, Ping Huang, Lucy Xi Lou, Xin-Yuan Fu, Colin J Barnstable","doi":"10.1007/s12177-011-9064-8","DOIUrl":null,"url":null,"abstract":"<p><p>The Müller cell is the only glial cell type generated from the retinal neuroepithelium. This cell type controls normal retina homeostasis and has been suggested to play a neuroprotective role. Recent evidence suggests that mammalian Müller cells can de-differentiate and return to a progenitor or stem cell stage following injury or disease. In vivo exploration of the molecular mechanisms of Müller cell differentiation and proliferation will add essential information to manipulate Müller cell functions. Signal transduction pathways that regulate Müller cell responses and activity are a critical part of their cellular machinery. In this study, we focus on mitogen-activated protein kinase (MAPK) signaling pathway during Müller glial cell differentiation and proliferation. We found that both MAPK and STAT3 signaling pathways are present during Müller glial cell development. Ciliary neurotrophic factor (CNTF)-stimulated Müller glial cell proliferation is associated with early developmental stages. Specific inhibition of MAPK phosphorylation significantly reduced the number of Müller glial cells with or without CNTF stimulation. These results suggested that the MAPK signal transduction pathway is important in the formation of Müller glial cells during retina development.</p>","PeriodicalId":73873,"journal":{"name":"Journal of ocular biology, diseases, and informatics","volume":"3 4","pages":"129-33"},"PeriodicalIF":0.0000,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12177-011-9064-8","citationCount":"6","resultStr":"{\"title\":\"MAPK signaling during Müller glial cell development in retina explant cultures.\",\"authors\":\"Samuel Shao-Min Zhang, Hong Li, Ping Huang, Lucy Xi Lou, Xin-Yuan Fu, Colin J Barnstable\",\"doi\":\"10.1007/s12177-011-9064-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The Müller cell is the only glial cell type generated from the retinal neuroepithelium. This cell type controls normal retina homeostasis and has been suggested to play a neuroprotective role. Recent evidence suggests that mammalian Müller cells can de-differentiate and return to a progenitor or stem cell stage following injury or disease. In vivo exploration of the molecular mechanisms of Müller cell differentiation and proliferation will add essential information to manipulate Müller cell functions. Signal transduction pathways that regulate Müller cell responses and activity are a critical part of their cellular machinery. In this study, we focus on mitogen-activated protein kinase (MAPK) signaling pathway during Müller glial cell differentiation and proliferation. We found that both MAPK and STAT3 signaling pathways are present during Müller glial cell development. Ciliary neurotrophic factor (CNTF)-stimulated Müller glial cell proliferation is associated with early developmental stages. Specific inhibition of MAPK phosphorylation significantly reduced the number of Müller glial cells with or without CNTF stimulation. These results suggested that the MAPK signal transduction pathway is important in the formation of Müller glial cells during retina development.</p>\",\"PeriodicalId\":73873,\"journal\":{\"name\":\"Journal of ocular biology, diseases, and informatics\",\"volume\":\"3 4\",\"pages\":\"129-33\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2010-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1007/s12177-011-9064-8\",\"citationCount\":\"6\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of ocular biology, diseases, and informatics\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1007/s12177-011-9064-8\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2011/8/12 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of ocular biology, diseases, and informatics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s12177-011-9064-8","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2011/8/12 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
MAPK signaling during Müller glial cell development in retina explant cultures.
The Müller cell is the only glial cell type generated from the retinal neuroepithelium. This cell type controls normal retina homeostasis and has been suggested to play a neuroprotective role. Recent evidence suggests that mammalian Müller cells can de-differentiate and return to a progenitor or stem cell stage following injury or disease. In vivo exploration of the molecular mechanisms of Müller cell differentiation and proliferation will add essential information to manipulate Müller cell functions. Signal transduction pathways that regulate Müller cell responses and activity are a critical part of their cellular machinery. In this study, we focus on mitogen-activated protein kinase (MAPK) signaling pathway during Müller glial cell differentiation and proliferation. We found that both MAPK and STAT3 signaling pathways are present during Müller glial cell development. Ciliary neurotrophic factor (CNTF)-stimulated Müller glial cell proliferation is associated with early developmental stages. Specific inhibition of MAPK phosphorylation significantly reduced the number of Müller glial cells with or without CNTF stimulation. These results suggested that the MAPK signal transduction pathway is important in the formation of Müller glial cells during retina development.