Jianhai Bai, Minli Zhang, Xiaomin Ding, Xingzhi Yang, Daniel Zheng, Hongyun Mou, Xiaoxiao Ruan, Yueqing Feng, Hai-xiong Han, Shi-li Wang
{"title":"微小RNA-21a-5p调节TGF-?靶向Smad7诱导1诱导的兔角膜细胞肌成纤维细胞转化","authors":"Jianhai Bai, Minli Zhang, Xiaomin Ding, Xingzhi Yang, Daniel Zheng, Hongyun Mou, Xiaoxiao Ruan, Yueqing Feng, Hai-xiong Han, Shi-li Wang","doi":"10.2306/scienceasia1513-1874.2022.011","DOIUrl":null,"url":null,"abstract":"The transforming growth factor β1 (TGF-β1)-induced transformation of keratocytes to myofibroblasts is a very common process during corneal wound healing, but a dysregulated TGF-β1 activity may induce unfavorable fibrosis and scar formation in the cornea. MicroRNA (miR)-21a-5p and Smad7 have been reported to play an important role in the fibrosis process. However, how miR-21a-5p involves in the TGF-β1-induced myofibroblasts transformation of keratocytes remains unclear. In the present study, we found an increase in the expressions of α-SMA and collagen I at protein level as well as Smad7 and miR-21a-5p at mRNA level when keratocytes were treated with TGF-β1Here; but the Smad7 at protein level kept unchanged. The overexpression of miR-21a-5p attenuated Smad7 protein expression, and miR-21a-5p inhibition promoted Smad7 protein expression without affecting its mRNA expression. Furthermore, inhibition of miR-21a-5p could decrease TGF-β1-inducedα-SMA expression, whereas the addition of Smad7 knockdown would rescue the expression of α-SMA. These results suggested that miR-21a-5p had a promoting effect on TGF-β1induced myofibroblast transformation of keratocytes by targeting Smad7 at its translation stage.","PeriodicalId":21577,"journal":{"name":"Scienceasia","volume":"1 1","pages":""},"PeriodicalIF":1.0000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"MicroRNA-21a-5p regulates TGF-?1-induced myofibroblast transformation of rabbit keratocytes by targeting Smad7\",\"authors\":\"Jianhai Bai, Minli Zhang, Xiaomin Ding, Xingzhi Yang, Daniel Zheng, Hongyun Mou, Xiaoxiao Ruan, Yueqing Feng, Hai-xiong Han, Shi-li Wang\",\"doi\":\"10.2306/scienceasia1513-1874.2022.011\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The transforming growth factor β1 (TGF-β1)-induced transformation of keratocytes to myofibroblasts is a very common process during corneal wound healing, but a dysregulated TGF-β1 activity may induce unfavorable fibrosis and scar formation in the cornea. MicroRNA (miR)-21a-5p and Smad7 have been reported to play an important role in the fibrosis process. However, how miR-21a-5p involves in the TGF-β1-induced myofibroblasts transformation of keratocytes remains unclear. In the present study, we found an increase in the expressions of α-SMA and collagen I at protein level as well as Smad7 and miR-21a-5p at mRNA level when keratocytes were treated with TGF-β1Here; but the Smad7 at protein level kept unchanged. The overexpression of miR-21a-5p attenuated Smad7 protein expression, and miR-21a-5p inhibition promoted Smad7 protein expression without affecting its mRNA expression. Furthermore, inhibition of miR-21a-5p could decrease TGF-β1-inducedα-SMA expression, whereas the addition of Smad7 knockdown would rescue the expression of α-SMA. These results suggested that miR-21a-5p had a promoting effect on TGF-β1induced myofibroblast transformation of keratocytes by targeting Smad7 at its translation stage.\",\"PeriodicalId\":21577,\"journal\":{\"name\":\"Scienceasia\",\"volume\":\"1 1\",\"pages\":\"\"},\"PeriodicalIF\":1.0000,\"publicationDate\":\"2022-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Scienceasia\",\"FirstCategoryId\":\"103\",\"ListUrlMain\":\"https://doi.org/10.2306/scienceasia1513-1874.2022.011\",\"RegionNum\":4,\"RegionCategory\":\"综合性期刊\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MULTIDISCIPLINARY SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Scienceasia","FirstCategoryId":"103","ListUrlMain":"https://doi.org/10.2306/scienceasia1513-1874.2022.011","RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MULTIDISCIPLINARY SCIENCES","Score":null,"Total":0}
MicroRNA-21a-5p regulates TGF-?1-induced myofibroblast transformation of rabbit keratocytes by targeting Smad7
The transforming growth factor β1 (TGF-β1)-induced transformation of keratocytes to myofibroblasts is a very common process during corneal wound healing, but a dysregulated TGF-β1 activity may induce unfavorable fibrosis and scar formation in the cornea. MicroRNA (miR)-21a-5p and Smad7 have been reported to play an important role in the fibrosis process. However, how miR-21a-5p involves in the TGF-β1-induced myofibroblasts transformation of keratocytes remains unclear. In the present study, we found an increase in the expressions of α-SMA and collagen I at protein level as well as Smad7 and miR-21a-5p at mRNA level when keratocytes were treated with TGF-β1Here; but the Smad7 at protein level kept unchanged. The overexpression of miR-21a-5p attenuated Smad7 protein expression, and miR-21a-5p inhibition promoted Smad7 protein expression without affecting its mRNA expression. Furthermore, inhibition of miR-21a-5p could decrease TGF-β1-inducedα-SMA expression, whereas the addition of Smad7 knockdown would rescue the expression of α-SMA. These results suggested that miR-21a-5p had a promoting effect on TGF-β1induced myofibroblast transformation of keratocytes by targeting Smad7 at its translation stage.
期刊介绍:
ScienceAsia is a multidisciplinary journal publishing papers of high quality bimonthly, in printed and electronic versions, by the Science Society of Thailand under Royal Patronage and the National Research Council of Thailand. The journal publishes original research papers that provide novel findings and important contribution to broad area in science and mathematics. Areas covered include Biological Sciences and Biotechnology, Chemistry and Material Sciences, Environmental and Applied Sciences, and Mathematics and Physical Sciences. Manuscripts may report scientifically useful data, observations or model predictions, and/or provide a new scientific concept or a new explanation of published results. Submissions of materials of current scientific interest are highly welcome, provided that there is sufficient scientific merit. The journal will not accept manuscripts which have been published or are being considered for publication elsewhere, nor should manuscripts being considered by ScienceAsia be submitted to other journals. Submitted manuscripts must conform to the guidelines given in the Instructions for Authors