Literature DB >> 27616193

RNCR3 knockdown inhibits diabetes mellitus-induced retinal reactive gliosis.

Chang Liu1, Chao-Peng Li2, Jia-Jian Wang3, Kun Shan1, Xin Liu4, Biao Yan5.   

Abstract

Retinal reactive gliosis is an important pathological feature of diabetic retinopathy. Identifying the underlying mechanisms causing reactive gliosis will be important for developing new therapeutic strategies for treating diabetic retinopathy. Herein, we show that long noncoding RNA-RNCR3 knockdown significantly inhibits retinal reactive gliosis. RNCR3 knockdown leads to a marked reduction in the release of several cytokines. RNCR3 knockdown alleviates diabetes mellitus-induced retinal neurodegeneration, as shown by less apoptotic retinal cells and ameliorative visual function. RNCR3 knockdown could also decrease Müller glial cell viability and proliferation, and reduce the expression of glial reactivity-related genes including GFAP and vimentin in vitro. Collectively, this study shows that RNCR3 knockdown may be a promising strategy for the prevention of diabetes mellitus-induced retinal neurodegeneration.
Copyright © 2016 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Diabetic retinopathy; Long noncoding RNA; Retinal reactive gliosis

Mesh:

Substances:

Year:  2016        PMID: 27616193     DOI: 10.1016/j.bbrc.2016.09.032

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


  14 in total

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