Open AccessRole of long non‐coding RNA MIAT in proliferation, apoptosis and migration of lens epithelial cells: a clinical and in vitro study
Author(s) -
Shen Yi,
Dong LingFeng,
Zhou RongMei,
Yao Jin,
Song YuChen,
Yang Hong,
Jiang Qin,
Yan Biao
Publication year - 2016
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12755
Subject(s) - gene knockdown , rna , long non coding rna , rna extraction , downregulation and upregulation , biology , apoptosis , microbiology and biotechnology , microrna , microarray analysis techniques , oxidative stress , cancer research , gene expression , gene , endocrinology , genetics
Age‐related cataract is among the most common chronic disorders of ageing and is the world's leading blinding disorder. Long non‐coding RNA s play important roles in several biological processes and complicated diseases. However, the role of lnc RNA s in the setting of cataract is still unknown. Here, we extracted total RNA s from the transparent and age‐matched cataractous human lenses, and determined lnc RNA expression profiles using microarray analysis. We found that 38 lnc RNA s were differentially expressed between transparent and cataractous lenses. 17 of 20 differentially expressed lnc RNA s were further verified by quantitative RT ‐ PCR s. One top abundant lnc RNA , MIAT , was specifically up‐regulated both in the plasma fraction of whole blood and aqueous humor of cataract patients. MIAT knockdown could affect the proliferation, apoptosis and migration of Human lens epithelial cells (HLECs) upon oxidative stress. Posterior capsule opacification ( PCO ) is a common complication of cataract surgery, which is associated with abnormal production of inflammatory factors. MIAT knockdown could repress tumour necrosis factor‐α‐induced abnormal proliferation and migration of HLEC s, suggesting a potential role of MIAT in PCO ‐related pathological process. Moreover, we found that MIAT acted as a ce RNA , and formed a feedback loop with Akt and miR‐150‐5p to regulate HLEC function. Collectively, this study provides a novel insight into the pathogenesis of age‐related cataract.