MiR-17-5p modulates osteoblastic differentiation and cell proliferation by targeting SMAD7 in non-traumatic osteonecrosis.
- Author:
Jie JIA
1
;
Xiaobo FENG
;
Weihua XU
;
Shuhua YANG
;
Qing ZHANG
;
Xianzhe LIU
;
Yong FENG
;
Zhipeng DAI
Author Information
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- MeSH: Adult; Base Sequence; Bone Morphogenetic Protein 2/metabolism; Cell Differentiation; Cell Line; Cell Proliferation; Female; *Gene Expression Regulation; Humans; Male; MicroRNAs/genetics/*metabolism; Middle Aged; Osteoarthritis/genetics/metabolism/pathology; Osteoblasts/*cytology/metabolism/*pathology; Osteogenesis; Osteonecrosis/*genetics/metabolism/pathology; Signal Transduction; Smad7 Protein/*genetics/metabolism; beta Catenin/metabolism
- From:Experimental & Molecular Medicine 2014;46(7):e107-
- CountryRepublic of Korea
- Language:English
- Abstract: MicroRNAs (miRNAs) have recently been recognized to have a role in human orthopedic disorders. The objective of our study was to explore the expression profile and biological function of miRNA-17-5p (miR-17-5p), which is well known to be related to cancer cell proliferation and invasion, in osteoblastic differentiation and in cell proliferation. The expression levels of miR-17-5p in the femoral head mesenchymal stem cells of 20 patients with non-traumatic osteonecrosis (ON) and 10 patients with osteoarthritis (OA) were examined by quantitative reverse transcription-PCR (qRT-PCR). Furthermore, the interaction between miR-17-5p and SMAD7 was observed. We found that in non-traumatic ON samples the level of mature miR-17-5p was significantly lower than that of OA samples (P=0.0002). By targeting SMAD7, miR-17-5p promoted nuclear translocation of beta-catenin, enhanced expression of COL1A1 and finally facilitated the proliferation and differentiation of HMSC-bm cells. We also demonstrated that restoring expression of SMAD7 in HMSC-bm cells partially reversed the function of miR-17-5p. Together, our data suggested a theory that dysfunction of a network containing miR-17-5p, SMAD7 and beta-catenin could contribute to ON pathogenesis. The present study prompts the potential clinical value of miR-17-5p in non-traumatic ON.
