Int J Sports Med
DOI: 10.1055/a-1342-7872
Genetics & Molecular Biology

MiR-30b-5p Influences Chronic Exercise Arthritic Injury by Targeting Hoxa1

Maoxun Li
1  Department of Orthopaedics, The People’s Hospital of Jimo.Qingdao, Qingdao, China
,
Fei Gai
2  Department of Radiotherapy, The People’s Hospital of Jimo.Qingdao, Qingdao, China
,
Hongyu Chen
3  Department of Emergency, Qingdao West Coast New Area Central Hospital, Qingdao, China
› Author Affiliations

Abstract

We identified the role of miR-30b-5p in chronic exercise arthritic injury. Rats with chronic exercise arthritic injury received treatment with miR-30b-5p antagomiR. H&E and Safranin O-fast green staining were performed. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were detected. The binding relationship between homeobox A1 (Hoxa1) and miR-30b-5p was revealed. After manipulating the expressions of miR-30b-5p and/or Hoxa1 in chondrocytes, the viability, apoptosis and migration of chondrocytes were assessed. The levels of molecules were determined by qRT-PCR or Western blot. MiR-30b-5p antagomiR ameliorated articular cartilage lesion and destruction, reduced Mankin’s score and the levels of TNF-α, IL-1β, miR-30b-5p, matrix metallopeptidase 13 (MMP-13), and cleaved caspase-3, and increased relative thickness and the levels of Hoxa1, Aggrecan and type II collagen (COLII) in model rats. MiR-30b-5p up-regulation decreased Hoxa1 level, viability, migration and induced apoptosis, whereas miR-30b-5p down-regulation produced the opposite effects. MiR-30b-5p up-regulation increased the levels of MMP-13 and cleaved caspase-3, but decreased those of Aggrecan and COLII in chondrocytes. However, the action of miR-30b-5p up-regulation on chondrocytes was reversed by Hoxa1 overexpression. In conclusion, miR-30b-5p is involved in cartilage degradation in rats with chronic exercise arthritic injury and regulates chondrocyte apoptosis and migration by targeting Hoxa1.



Publication History

Received: 26 August 2020

Accepted: 14 December 2020

Publication Date:
30 April 2021 (online)

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