miR-486-5p attenuates steroid-induced adipogenesis and osteonecrosis of the femoral head via TBX2/P21 axis.
Yu ChenBoyu TangWeiqian JiangMingjie SunHongrui ZhangYuzhang TaoHongwei WangDulei XiangHaobo BaiMingkang GuoPei ZhaoWenlong YanXiao HuangTingmei ChenChengjie LianJian ZhangPublished in: Stem cells (Dayton, Ohio) (2023)
Enhanced adipogenic differentiation of mesenchymal stem cells (MSCs) is considered as a major risk factor of steroid-induced osteonecrosis of the femoral head (SOFNH). The role of microRNAs during this process has sparked interest. miR-486-5p expression was down-regulated significantly in femoral head bone tissues of both SONFH patients and rat model. The purpose of this study was to reveal the role of miR-486-5p on MSCs adipogenesis and SONFH progression. The present study showed that miR-486-5p could significantly inhibit adipogenesis of 3T3-L1 cells by suppressing mitotic clonal expansion (MCE). And up-regulated expression of P21, which was caused by miR-486-5p mediated TBX2 decrease, was responsible for inhibited MCE. Further, miR-486-5p was demonstrated to effectively inhibit steroid-induced fat formation in the femoral head and prevented SONFH progression in a rat model. Considering the potent effects of miR-486-5p on attenuating adipogenesis, it seems to be a promising target for the treatment of SONFH.
Keyphrases
- mesenchymal stem cells
- high glucose
- diabetic rats
- poor prognosis
- umbilical cord
- end stage renal disease
- drug induced
- transcription factor
- adipose tissue
- risk factors
- newly diagnosed
- induced apoptosis
- prognostic factors
- high fat diet induced
- stem cells
- cell proliferation
- long non coding rna
- endothelial cells
- signaling pathway
- peritoneal dialysis
- anti inflammatory
- cell cycle
- dna methylation
- cell cycle arrest
- soft tissue
- smoking cessation
- patient reported outcomes
- endoplasmic reticulum stress