Knockdown of LncRNA H19 Relieves LPS-Induced Damage by Modulating miR-130a in Osteoarthritis
10.3349/ymj.2019.60.4.381
- Author:
Yi HU
1
;
Sukai LI
;
Yonggen ZOU
Author Information
1. Department of Orthopedics, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, China. w0309211@sina.com
- Publication Type:Original Article
- Keywords:
Osteoarthritis;
lipopolysaccharide;
lncRNA H19;
miR-130a
- MeSH:
Apoptosis;
Binding Sites;
Cell Survival;
Flow Cytometry;
Luciferases;
Osteoarthritis;
Polymerase Chain Reaction;
Porifera;
RNA;
RNA, Long Noncoding;
Sincalide
- From:Yonsei Medical Journal
2019;60(4):381-388
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Osteoarthritis (OA) is a commonly occurring illness without a definitive cure, at present. Long non-coding RNAs (lncRNAs) have been widely confirmed to be involved in the modulation of OA progression. This study aimed to investigate the role and mechanism of lncRNA H19 in OA. MATERIALS AND METHODS: Abundances of H19 and microRNA-130a (miR-130a) in lipopolysaccharide (LPS)-treated C28/I2 cells were measured by reverse-transcription quantitative PCR (RT-qPCR). CCK-8 and flow cytometry analyses were carried out to assess cell viability and apoptosis. Starbase online software was used to predict the putative binding sites between H19 and miR-130a. Luciferase reporter, RNA pull down, and RT-qPCR were performed to analyze the true interaction between H19 and miR-130a. RESULTS: A notably dose-dependent elevation of H19 levels was observed in LPS-treated C28/I2 cells. Knockdown of H19 ameliorated the injury of LPS-induced C28/I2 cells, reflected by induced viability, decreased apoptosis, and reduced inflammatory factor secretions. Moreover, H19 negatively regulated the expression of miR-130a via acting as a molecular sponge for miR-130a. The stimulatory effects of H19 on cell damage were abolished following the restoration of miR-130a. CONCLUSION: LncRNA H19 aggravated the injury of LPS-induced C28/I2 cells by sponging miR-130a, hinting a novel regulatory mechanism and a potential therapeutic target for OA.
