MicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic Cataracts Through Targeting SNAI1

Abstract Epithelial-mesenchymal transition (EMT) is a highly conserved and fundamental process in development, fibrosis, and metastasis. During the process, epithelial cells lose their morphology and transcriptional program, and transdifferentiate to mesenchymal cells. It has been reported that lens...

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Autores principales:	Lu Zhang, Ye Wang, Wenfeng Li, Panagiotis A. Tsonis, Zhiyuan Li, Lixin Xie, Yusen Huang
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/eb04a95bda76494f9b547cd18eda4401
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spelling	oai:doaj.org-article:eb04a95bda76494f9b547cd18eda44012021-12-02T15:06:09ZMicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic Cataracts Through Targeting SNAI110.1038/s41598-017-01320-32045-2322https://doaj.org/article/eb04a95bda76494f9b547cd18eda44012017-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-01320-3https://doaj.org/toc/2045-2322Abstract Epithelial-mesenchymal transition (EMT) is a highly conserved and fundamental process in development, fibrosis, and metastasis. During the process, epithelial cells lose their morphology and transcriptional program, and transdifferentiate to mesenchymal cells. It has been reported that lens epithelial cells undergo EMT during cataract formation, and regulation of microRNAs on genes is associated with lens development. However, the molecular mechanisms of this regulation in diabetic cataract still need to be investigated. In the present study, the expression of E-cadherin was downregulated, while the expression of alpha-SMA and vimentin was upregulated in diabetic cataract tissues and the in vitro model, suggesting the involvement of EMT in diabetic cataract formation. Results of miRNA profiling demonstrated that miR-30a was markedly downregulated in diabetic cataract tissues. Overexpression of miR-30a-5p decreased SNAI1, a known modulator of EMT, and the expression of vimentin and alpha-SMA in our diabetic cataract model in vitro. It is concluded that EMT is involved in human diabetic cataract, and upregulation of miR-30a can repress EMT through its targeting of SNAI1 in lens epithelial cells, which make miR-30a a novel target of therapeutic intervention for human diabetic cataract.Lu ZhangYe WangWenfeng LiPanagiotis A. TsonisZhiyuan LiLixin XieYusen HuangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-7 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Lu Zhang Ye Wang Wenfeng Li Panagiotis A. Tsonis Zhiyuan Li Lixin Xie Yusen Huang MicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic Cataracts Through Targeting SNAI1
description	Abstract Epithelial-mesenchymal transition (EMT) is a highly conserved and fundamental process in development, fibrosis, and metastasis. During the process, epithelial cells lose their morphology and transcriptional program, and transdifferentiate to mesenchymal cells. It has been reported that lens epithelial cells undergo EMT during cataract formation, and regulation of microRNAs on genes is associated with lens development. However, the molecular mechanisms of this regulation in diabetic cataract still need to be investigated. In the present study, the expression of E-cadherin was downregulated, while the expression of alpha-SMA and vimentin was upregulated in diabetic cataract tissues and the in vitro model, suggesting the involvement of EMT in diabetic cataract formation. Results of miRNA profiling demonstrated that miR-30a was markedly downregulated in diabetic cataract tissues. Overexpression of miR-30a-5p decreased SNAI1, a known modulator of EMT, and the expression of vimentin and alpha-SMA in our diabetic cataract model in vitro. It is concluded that EMT is involved in human diabetic cataract, and upregulation of miR-30a can repress EMT through its targeting of SNAI1 in lens epithelial cells, which make miR-30a a novel target of therapeutic intervention for human diabetic cataract.
format	article
author	Lu Zhang Ye Wang Wenfeng Li Panagiotis A. Tsonis Zhiyuan Li Lixin Xie Yusen Huang
author_facet	Lu Zhang Ye Wang Wenfeng Li Panagiotis A. Tsonis Zhiyuan Li Lixin Xie Yusen Huang
author_sort	Lu Zhang
title	MicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic Cataracts Through Targeting SNAI1
title_short	MicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic Cataracts Through Targeting SNAI1
title_full	MicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic Cataracts Through Targeting SNAI1
title_fullStr	MicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic Cataracts Through Targeting SNAI1
title_full_unstemmed	MicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic Cataracts Through Targeting SNAI1
title_sort	microrna-30a regulation of epithelial-mesenchymal transition in diabetic cataracts through targeting snai1
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/eb04a95bda76494f9b547cd18eda4401
work_keys_str_mv	AT luzhang microrna30aregulationofepithelialmesenchymaltransitionindiabeticcataractsthroughtargetingsnai1 AT yewang microrna30aregulationofepithelialmesenchymaltransitionindiabeticcataractsthroughtargetingsnai1 AT wenfengli microrna30aregulationofepithelialmesenchymaltransitionindiabeticcataractsthroughtargetingsnai1 AT panagiotisatsonis microrna30aregulationofepithelialmesenchymaltransitionindiabeticcataractsthroughtargetingsnai1 AT zhiyuanli microrna30aregulationofepithelialmesenchymaltransitionindiabeticcataractsthroughtargetingsnai1 AT lixinxie microrna30aregulationofepithelialmesenchymaltransitionindiabeticcataractsthroughtargetingsnai1 AT yusenhuang microrna30aregulationofepithelialmesenchymaltransitionindiabeticcataractsthroughtargetingsnai1
_version_	1718388616906932224

MicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic Cataracts Through Targeting SNAI1

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