ATP6V1H regulates the growth and differentiation of bone marrow stromal cells

Journal Article · Sun Jul 15 04:00:00 EDT 2018 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/J.BBRC.2018.05.124· OSTI ID:23105752

Li, Lin ^[1]; Yang, Shaoqing; Zhang, Yanli; Ji, Dongrui ^[1]; Jin, Zuolin ^[2]; Duan, Xiaohong ^[1]

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1. 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 (China)
2. 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 (China)

Highlights: • Lack of ATP6V1H inhibits the proliferation of bone marrow stromal cells (BMSCs). • Partial loss of ATP6V1H inhibits osteogenic differentiation and promotes adipogenic differentiation of BMSCs. • ATP6V1H interacts with TGF-β receptor I and AP-2 complex to regulate the proliferation and differentiation of BMSCs. 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{sup +/-} 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{sup +/-} 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.

• OSTI ID: 23105752
• Journal Information: Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 1 Vol. 502; ISSN BBRCA9; ISSN 0006-291X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
BONE MARROW
CELL CYCLE
MESSENGER-RNA
MICE
RECEPTORS