ATP6V1H 调控骨髓基质细胞的生长和分化。
ATP6V1H regulates the growth and differentiation of bone marrow stromal cells.
机构信息
State Key Laboratory of Military Stomatology, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Oral Diseases, Department of Oral Biology, School of Stomatology, The Fourth Military Medical University, 145 West Changle Road, Xi'an, Shaanxi, 710032, PR China; State Key Laboratory of Military Stomatology, Department of Orthodontics School of Stomatology, The Fourth Military Medical University, 145 West Changle Road, Xi'an, Shaanxi, 710032, PR China.
State Key Laboratory of Military Stomatology, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Oral Diseases, Department of Oral Biology, School of Stomatology, The Fourth Military Medical University, 145 West Changle Road, Xi'an, Shaanxi, 710032, PR China.
出版信息
Biochem Biophys Res Commun. 2018 Jul 7;502(1):84-90. doi: 10.1016/j.bbrc.2018.05.124. Epub 2018 May 25.
ATP6V1H encodes subunit H of vacuolar ATPase (V-ATPase) and may regulate osteoclastic function. The deficiency of ATP6V1H caused bone loss in human, mouse and zebrafish. In this report, we identified the mechanisms by which ATP6V1H regulates proliferation and differentiation of bone marrow stromal cells (BMSCs). We found that ATP6V1H was expressed in BMSCs, and Atp6v1h BMSCs exhibited the lower proliferation rate, cell cycle arrest and reduced osteogenic differentiation capacity, as well as the increased adipogenic potentials. Histologic analysis confirmed less bone formation and more fatty degeneration in Atp6v1h mice in the different age groups. Q-PCR analysis revealed that loss of ATP6V1H function downregulated the mRNA level of TGF-β1 receptor, and its binding molecule, subunit β of adaptor protein complex 2 (AP-2), suggesting ATP6V1H regulates the proliferation and differentiation of BMSCs by interacting with TGF-β receptor I and AP-2 complex.
ATP6V1H 编码液泡型 ATP 酶（V-ATPase）亚基 H，可能调节破骨细胞功能。ATP6V1H 的缺乏导致人类、小鼠和斑马鱼的骨丢失。在本报告中，我们确定了 ATP6V1H 调节骨髓基质细胞（BMSCs）增殖和分化的机制。我们发现 ATP6V1H 在 BMSCs 中表达，并且 Atp6v1h BMSCs 表现出较低的增殖率、细胞周期停滞和减少的成骨分化能力，以及增加的成脂潜力。组织学分析证实，在不同年龄组的 Atp6v1h 小鼠中，骨形成减少，脂肪变性增加。Q-PCR 分析显示，ATP6V1H 功能丧失下调了 TGF-β1 受体及其结合分子衔接蛋白复合物 2（AP-2）亚基 β 的 mRNA 水平，表明 ATP6V1H 通过与 TGF-β 受体 I 和 AP-2 复合物相互作用来调节 BMSCs 的增殖和分化。
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