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Long non‐coding RNA RP11‐820 promotes extracellular matrix production via regulating miR‐3178/MYOD1 in human trabecular meshwork cells
Author(s) -
Shen Wencui,
Huang Bingqing,
He Ye,
Shi Liukun,
Yang Jin
Publication year - 2020
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.15058
Subject(s) - extracellular matrix , trabecular meshwork , downregulation and upregulation , microbiology and biotechnology , gene , biology , extracellular , oxidative stress , rna , glaucoma , genetics , neuroscience , endocrinology
Primary open angle glaucoma (POAG) is the most common type of glaucoma. At the mechanistic level, POAG is thought to be caused by extracellular matrix (ECM) deposition in the trabecular meshwork (TM). Growing evidence has shown that long noncoding RNAs (lncRNAs) are involved in the fibrotic process underlying many diseases. This study was undertaken to explore the role of lncRNA‐RP11‐820 in ECM production of human TM cells (HTMCs). Our results revealed that lncRNA‐RP11‐820 was significantly upregulated under oxidative stress in HTMCs. Further investigation revealed that lncRNA‐RP11‐820 directly binds miR‐3178, through which the expression of MYOD1 is regulated. Importantly, MYOD1 can transcriptionally activate ECM genes in HTMCs, in complex with STAT3. Taken together, our data established that oxidative stress‐induced lncRNA‐RP11‐820 plays a key role in regulating the miR‐3178/MYOD1/ECM axis in HTMCs. These findings further elucidate the pathogenic mechanism and provide a novel therapeutic target relevant to POAG.