RETRACTED: miRNA-187-5p Regulates Osteoblastic Differentiation of Bone Marrow Mesenchymal Stem Cells in Mice by Targeting ICAM1 (Retracted Article)

被引:12
|
作者
Sun, Yi [1 ]
Wang, Xin [2 ]
Chen, Guanghua [1 ]
Song, Chengchao [1 ]
Ma, Xinnan [1 ]
Fu, Yutuo [3 ]
Feng, Chao [4 ]
Yan, Jinglong [1 ]
机构
[1] Harbin Med Univ, Affiliated Hosp 2, Dept Orthopaed, 148 Baojian Rd, Harbin 150081, Peoples R China
[2] Harbin Med Univ, Phys Educ & Res Off, Harbin 150081, Peoples R China
[3] Heilongjiang Prov Hosp, Dept Orthopaed, Harbin 150010, Peoples R China
[4] Harbin Med Univ, Dept Pharmacol, Harbin 150081, Peoples R China
关键词
INTERCELLULAR-ADHESION MOLECULE-1; OSTEOGENIC DIFFERENTIATION; APOPTOSIS; GROWTH; MIR-187-5P; RISK;
D O I
10.1155/2020/6139469
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Osteoporosis (OP) is a common bone metabolic disease, the process of which is fundamentally irreversible. Therefore, the investigation into osteoblastic differentiation of bone marrow mesenchymal stem cells (BMSCs) will provide more clues for OP treatment. In the present study, we found that microRNA-187-5p (miR-187-5p) played a key role on osteoblastic differentiation, which was significantly upregulated during osteogenic differentiation of BMSCs in mice. Moreover, overexpression of miR-187-5p suppressed osteoblastic differentiation of BMSCs through increasing alkaline phosphatase (ALP), matrix mineralization, and levels of Osterix (OSX), and osteopontin (OPN) as well as runt-related transcription factor 2 (Runx2) in vitro. The results in vivo indicated that the upregulation of miR-187-5p enhanced the efficacy of new bone formation in the heterotopic bone formation assay. Luciferase reporter assay and western blot analysis revealed that miR-187-5p was involved in osteogenesis by targeting intracellular adhesion molecule 1 (ICAM-1). Furthermore, ICAM-1 silence inhibited osteoblastic differentiation of BMSCs. Taken together, our results suggested for the first time that miR-187-5p may promote osteogenesis by targeting ICAM-1, and provided a possible therapeutic target for bone metabolic diseases.
引用
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页数:12
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