Abstract:
:Fracture healing is a repair process of a mechanical discontinuity loss of force transmission, and pathological mobility of bone. Increasing evidence suggests that microRNA (miRNA) could regulate chondrocyte, osteoblast, and osteoclast differentiation and function, indicating miRNA as key regulators of bone formation, resorption, remodeling, and repair. Hence, during this study, we established a right femur fracture mouse model to explore the effect microRNA-185 (miR-185) has on osteoblasts in mice during fracture healing and its underlying mechanism. After successfully model establishment, osteoblasts were extracted and treated with a series of mimics or inhibitors of miR-185, or siRNA against PTH. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot analysis were performed to determine the levels of miR-185, PTH, β-catenin and Wnt5b. Cell viability, cycle distribution and apoptosis were detected by means of MTT and flow cytometry assays. Dual luciferase reporter gene assay verified that PTH is a target gene of miR-185. Osteoblasts transfected with miR-185 mimics or siRNA against PTH presented with decreased levels of PTH, β-catenin and Wnt5b which indicated that miR-185 blocks the Wnt/β -catenin axis by inhibiting PTH. Moreover, miR-185 inhibitors promoted the osteoblast viability and reduced apoptosis with more cells arrested at the G1 stage. MiR-185 mimics were observed to have inhibitory effects on osteoblasts as opposed to those induced by miR-185 inhibitors. Above key results indicated that suppression of miR-185 targeting PTH could promote osteoblast growth and proliferation in mice during fracture healing through activating Wnt/β -catenin axis.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Yao CJ,Lv Y,Zhang CJ,Jin JX,Xu LH,Jiang J,Geng B,Li H,Xia YY,Wu Mdoi
10.1016/j.bbrc.2018.04.138subject
Has Abstractpub_date
2018-06-18 00:00:00pages
55-63issue
1eissn
0006-291Xissn
1090-2104pii
S0006-291X(18)30919-7journal_volume
501pub_type
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