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miR‐182‐5p overexpression inhibits chondrogenesis by down‐regulating PTHLH
Author(s) -
Bai Ming,
Yin Heping,
Zhao Jian,
Li Yang,
Wu Yimin
Publication year - 2019
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11047
Subject(s) - chondrogenesis , downregulation and upregulation , chemistry , microbiology and biotechnology , reporter gene , microrna , mesenchymal stem cell , cancer research , gene expression , gene , biology , biochemistry
Human bone marrow mesenchymal stem cells (hBM‐MSC) have the ability of differentiating into chondrocytes and osteoblasts. miR‐182‐5p promotes osteoclastogenesis and bone metastasis by up‐regulating the expression of parathyroid hormone‐like hormone (PTHLH). However, the function of miR‐182‐5p in chondrogenesis is still unknown. Mimic or inhibitor of miR‐182‐5p was used to upregulate or knock‐down miR‐182‐5p expression, respectively. We analyzed chondrogenesis by Safranin O staining and Blyscan™ Sulfated Glycosaminoglycan Assay. Immunohistochemistry, real‐time PCR, and Western bolts were used to detect related makers. miR‐182‐5p overexpression inhibited chondrogenesis. Dual‐luciferase reporter assay indicated that PTHLH was one of the target genes of miR‐182‐5p. Further studies showed that miR‐182‐5p overexpression down‐regulated the expression of SOX‐9 and COL2A1, but up‐regulated COL1A1 and COL10A1. Consistently, miR‐182‐5p knock‐down had the opposite effects. This effect of miR‐182‐5p in BM‐MSCs can be rescued by PTHLH overexpression. miR‐182‐5p may play a negative role in chondrogenesis by down‐regulating PTHLH.