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Adipose mesenchymal stem cells‐secreted extracellular vesicles containing microRNA‐192 delays diabetic retinopathy by targeting ITGA1
Author(s) -
Gu Cao,
Zhang Hongjun,
Gao Yu
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.30213
Subject(s) - angiogenesis , mesenchymal stem cell , diabetic retinopathy , microbiology and biotechnology , microvesicles , gene knockdown , retinal pigment epithelium , retinal , cancer research , microrna , medicine , chemistry , biology , diabetes mellitus , endocrinology , ophthalmology , apoptosis , biochemistry , gene
Diabetic retinopathy (DR) has characteristics of early loss of capillary pericytes, contributing to aberrant endothelial proliferation and angiogenesis. The function of extracellular vesicles (Evs) derived from mesenchymal stem cells (MSCs) in angiogenesis and endothelial proliferation were investigated in the present study. In particular, the role of microRNA‐192 (miR‐192) was described. Firstly, the GSE60436 data set was applied to screen out that integrin subunit α1 (ITGA1) was overexpressed in DR. Subsequently, streptozotocin (STZ) was used to induce diabetes in rats, which was later subjected to intravitreal injection of targeted shRNAs. ITGA1 knockdown alleviated inflammation and angiogenesis in STZ‐induced diabetic retina. Evs were extracted from MSCs and injected into rat vitreous. Meanwhile, human retinal microvascular endothelial cells, Müller cells, and retinal pigment epithelium cells were exposed to high glucose. MSC‐derived Evs relieved inflammatory response and angiogenesis by shuttling miR‐192. miR‐192 targeted and negatively regulated ITGA1, thereby ameliorating diabetic retinal damage. Our study established that miR‐192 released by Evs from MSCs could delay the events of the inflammatory response and angiogenesis in DR and may represent a possible therapeutic approach for the treatment of DR.