{"title":"长链非编码rna - x失活特异性转录物通过上调miR-36促进视神经挤压损伤后视网膜神经节细胞存活","authors":"Qingjia Ren, Junjun Zhang","doi":"10.1166/jbt.2023.3265","DOIUrl":null,"url":null,"abstract":"Retinal ganglion cells (RGC) axons participate in the construction of optic nerve, and prevent the damage of RGC during acute optic nerve injury. IncRNA-XIST is crucial for RGC apoptosis. Our study intends to assess IncRNA-XIST’s role in the regulation of RGC apoptosis in an attempt\n to provide a theoretical basis for treating optic nerve crush injury. Two genotypes of mice (wild-type and miR-36 KO) were used to establish an optic nerve crush injury model to investigate the regulatory role of IncRNA-XIST gene in RGCs apoptosis. These mice were then randomly assigned into\n control group (WT), injury group, and XIST/injury group. The changes of apoptotic genes and proteins in retinal ganglion cells were analyzed by qPCR, WB and TUNEL staining. In wild-type mice, RGC apoptosis was significantly increased after optic nerve compression injury, and the expression\n of Bax and Bad was significantly increased. When the LncRNA-XIST gene was overexpressed before retinal crush injury, the apoptosis of retinal ganglion cells was significantly reduced, and Bax and Bad levels were decreased as compared with model group of optic nerve injury. The results showed\n that in wild-type mice, overexpression of IncRNA-XIST gene promoted the survival of RGC after optic nerve crush injury. In addition, upregulation of IncRNA-xist expression in miR-36 KO mice did not reduce retinal ganglion cell apoptosis and alter the apoptotic protein expression after optic\n nerve crush injury. Defects of miR-36 alone or overexpression of XIST gene do not cause morphological damage of retina in mice. In mouse ganglion cells, miR-36 expression was up-regulated in both injured cells and overexpressed XIST gene. However, up-regulation of miR-36 caused by overexpression\n of XIST gene was more obvious. In addition, in vivo studies of wild-type mice, it was found that overexpression of XIST reduced retinal ganglion cell apoptosis, and this effect was abolished in miR-36 KO mice. In conclusion, lncRNA-XIST reduces ganglion cell apoptosis by upregulating\n miR-36 and promotes the survival of RGC after nerve crush injury.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1000,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Long Non-Coding RNA-X-Inactive Specific Transcript Promotes the Retinal Ganglion Cell Survival After Optic Nerve Crush Injury by Upregulating miR-36\",\"authors\":\"Qingjia Ren, Junjun Zhang\",\"doi\":\"10.1166/jbt.2023.3265\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Retinal ganglion cells (RGC) axons participate in the construction of optic nerve, and prevent the damage of RGC during acute optic nerve injury. IncRNA-XIST is crucial for RGC apoptosis. Our study intends to assess IncRNA-XIST’s role in the regulation of RGC apoptosis in an attempt\\n to provide a theoretical basis for treating optic nerve crush injury. Two genotypes of mice (wild-type and miR-36 KO) were used to establish an optic nerve crush injury model to investigate the regulatory role of IncRNA-XIST gene in RGCs apoptosis. These mice were then randomly assigned into\\n control group (WT), injury group, and XIST/injury group. The changes of apoptotic genes and proteins in retinal ganglion cells were analyzed by qPCR, WB and TUNEL staining. In wild-type mice, RGC apoptosis was significantly increased after optic nerve compression injury, and the expression\\n of Bax and Bad was significantly increased. When the LncRNA-XIST gene was overexpressed before retinal crush injury, the apoptosis of retinal ganglion cells was significantly reduced, and Bax and Bad levels were decreased as compared with model group of optic nerve injury. The results showed\\n that in wild-type mice, overexpression of IncRNA-XIST gene promoted the survival of RGC after optic nerve crush injury. In addition, upregulation of IncRNA-xist expression in miR-36 KO mice did not reduce retinal ganglion cell apoptosis and alter the apoptotic protein expression after optic\\n nerve crush injury. Defects of miR-36 alone or overexpression of XIST gene do not cause morphological damage of retina in mice. In mouse ganglion cells, miR-36 expression was up-regulated in both injured cells and overexpressed XIST gene. However, up-regulation of miR-36 caused by overexpression\\n of XIST gene was more obvious. In addition, in vivo studies of wild-type mice, it was found that overexpression of XIST reduced retinal ganglion cell apoptosis, and this effect was abolished in miR-36 KO mice. In conclusion, lncRNA-XIST reduces ganglion cell apoptosis by upregulating\\n miR-36 and promotes the survival of RGC after nerve crush injury.\",\"PeriodicalId\":15300,\"journal\":{\"name\":\"Journal of Biomaterials and Tissue Engineering\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.1000,\"publicationDate\":\"2023-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Biomaterials and Tissue Engineering\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1166/jbt.2023.3265\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biomaterials and Tissue Engineering","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1166/jbt.2023.3265","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Long Non-Coding RNA-X-Inactive Specific Transcript Promotes the Retinal Ganglion Cell Survival After Optic Nerve Crush Injury by Upregulating miR-36
Retinal ganglion cells (RGC) axons participate in the construction of optic nerve, and prevent the damage of RGC during acute optic nerve injury. IncRNA-XIST is crucial for RGC apoptosis. Our study intends to assess IncRNA-XIST’s role in the regulation of RGC apoptosis in an attempt
to provide a theoretical basis for treating optic nerve crush injury. Two genotypes of mice (wild-type and miR-36 KO) were used to establish an optic nerve crush injury model to investigate the regulatory role of IncRNA-XIST gene in RGCs apoptosis. These mice were then randomly assigned into
control group (WT), injury group, and XIST/injury group. The changes of apoptotic genes and proteins in retinal ganglion cells were analyzed by qPCR, WB and TUNEL staining. In wild-type mice, RGC apoptosis was significantly increased after optic nerve compression injury, and the expression
of Bax and Bad was significantly increased. When the LncRNA-XIST gene was overexpressed before retinal crush injury, the apoptosis of retinal ganglion cells was significantly reduced, and Bax and Bad levels were decreased as compared with model group of optic nerve injury. The results showed
that in wild-type mice, overexpression of IncRNA-XIST gene promoted the survival of RGC after optic nerve crush injury. In addition, upregulation of IncRNA-xist expression in miR-36 KO mice did not reduce retinal ganglion cell apoptosis and alter the apoptotic protein expression after optic
nerve crush injury. Defects of miR-36 alone or overexpression of XIST gene do not cause morphological damage of retina in mice. In mouse ganglion cells, miR-36 expression was up-regulated in both injured cells and overexpressed XIST gene. However, up-regulation of miR-36 caused by overexpression
of XIST gene was more obvious. In addition, in vivo studies of wild-type mice, it was found that overexpression of XIST reduced retinal ganglion cell apoptosis, and this effect was abolished in miR-36 KO mice. In conclusion, lncRNA-XIST reduces ganglion cell apoptosis by upregulating
miR-36 and promotes the survival of RGC after nerve crush injury.