RETRACTED ARTICLE: Down-regulated microRNA-141 facilitates osteoblast activity and inhibits osteoclast activity to ameliorate osteonecrosis of the femoral head via up-regulating TGF-β2

Abstract

Osteonecrosis of the femoral head (ONFH) is a pathological process that initially occurs in the weight-bearing field of the femoral head. Due to the unknown pathogenesis, this study was for the investigation of the effect of microRNA-141 (miR-141) targeting transforming growth factor-β2 (TGF-β2) on regulating osteoblast activity and osteoclast activity in steroid-induced ONFH.Tissues of ONFH and normal femoral head were collected for detecting the expression of miR-141 and TGF-β2. A rat model of ONFH was constructed by injection of hormones, and transfected with miR-141 inhibitors and overexpressed TGF-β2. The apoptosis of bone cells was detected by TUNEL staining. The expression of osteoprotegerin (OPG), osteoprotegerin ligand (OPGL), Bcl-2, Bax, Runx2, BMP2 and RANK were detected.Highly expressed miR-141 and lowly expressed TGF-β2 existed in femoral head tissues in ONFH. Inhibited miR-141 resulted in elevated TGF-β2 in femoral head tissues in ONFH of rats. Depressed miR-141 or overexpressed TGF-β2 inhibited the apoptosis of bone cells of rats with ONFH and induced elevated OPG, Bcl-2, BMP2, Runx2 and declined OPGL, Bax and RANK expression in the femoral head tissues of rats with ONFH.Altogether, we find that down-regulated miR-141 promotes osteoblast activity and inhibits osteoclast activity to ameliorate ONFH via up-regulated TGF-β2 expression.

The role of biomechanical forces and MALAT1/miR‐329‐5p/PRIP signalling on glucocorticoid‐induced osteonecrosis of the femoral head

“…Abnormal bone metabolism is one theory for the pathogenesis of GIONFH. Previous studies have usually focused on either osteoclasts or osteoblasts since these cells are regulated through different signalling pathways 10,22‐24 . Our study is the first to assess the effect of concurrent osteoclast and osteoblast differentiation on GIONFH through the expression of PRIP protein.…”

“…Previous studies have usually focused on either osteoclasts or osteoblasts since these cells are regulated through different signalling pathways. 10,[22][23][24] Our study is the first to assess the effect of concurrent osteoclast and osteoblast differentiation on GIONFH through the expression of PRIP protein. In our study, the expression of PRIP was up-regulated in the GIONFH and GIONFH_Treadmill groups in vivo, and when RAW264.7 cells or MC3T3E1 cells were treated with dexamethasone in vitro.…”

GINS2 affects activity/differentiation, apoptosis and proliferation of osteoblast and osteoclast in steroid-induced osteonecrosis of the femoral head by regulating P53/GADD45A signaling pathway

“…Mice were randomly divided into 2 groups: normal control group (NC, n = 10) and the model group (n = 10). The mice in the model group were received intramuscular injection of Prednisolone Acetate (49 mg/kg) while the mice in the NC group were received equivalent saline injection daily with once a day for 6 d (Tian et al, 2020). On the 7th day of model establishment, all mice were executed by breaking neck, and the femoral tissues were taken and reserved in ultralow freezer at -80 °C for later use.…”

“…Moreover, during bone formation, osteoblasts must go through four phases: cell proliferation and differentiation, extracellular matrix maturation, extracellular matrix mineralization and apoptosis. Recently, Tian et al (2020) found that enhancement of osteoblast activity and depression of osteoclast activity can ameliorate ONFH. These evidences indicate that the proliferation, differentiation/activity, apoptosis of osteoclasts and osteoblasts may affect the occurrence and development of SINFH.…”

“…Hence, maintaining the proportional balance between osteoblasts and osteoclasts may be one of the pivotal factors in the treatment of ONFH. Previous study has reported that the promotion of osteoblast activity and inhibition of osteoclast activity contribute to the improvement of ONFH (Tian et al, 2020). Furthermore, proosteoblast (bone progenitor cell) can differentiate into osteoblast and mononuclear macrophage can differentiate into osteoclast, and osteoblast is need to undergo four stages of osteoblast proliferation, extracellular matrix maturation, extracellular matrix mineralization and osteoblast apoptosis during bone formation.…”