2. Academic Validation
  3. Microfibrillar-associated protein 5 suppresses adipogenesis by inhibiting essential coactivator of PPARγ

Microfibrillar-associated protein 5 suppresses adipogenesis by inhibiting essential coactivator of PPARγ

  • Sci Rep. 2023 Apr 5;13(1):5589. doi: 10.1038/s41598-023-32868-y.
Tianlong Zhang # 1 2,  Haoran Li # 1 3,  Shiwei Sun 1 2,  Wuling Zhou 1 2,  Tieqi Zhang 1 2,  Yueming Yu 1 2,  Qiang Wang 4 5,  Minghai Wang 6 7
Affiliations

Affiliations

  • 1 Department of Orthopedics, Shanghai Fifth People's Hospital, Fudan University, No128. Ruili Road, Minhang District, Shanghai, 200240, China.
  • 2 Center of Community-Based Health Research, Fudan University, Shanghai, China.
  • 3 Department of Anatomy and Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
  • 4 Department of Orthopedics, Shanghai Fifth People's Hospital, Fudan University, No128. Ruili Road, Minhang District, Shanghai, 200240, China. [email protected].
  • 5 Center of Community-Based Health Research, Fudan University, Shanghai, China. [email protected].
  • 6 Department of Orthopedics, Shanghai Fifth People's Hospital, Fudan University, No128. Ruili Road, Minhang District, Shanghai, 200240, China. [email protected].
  • 7 Center of Community-Based Health Research, Fudan University, Shanghai, China. [email protected].
  • # Contributed equally.
PMID: 37020143 DOI: 10.1038/s41598-023-32868-y
Abstract

Femoral head necrosis is responsible for severe pain and its incidence is increasing. Abnormal adipogenic differentiation and fat cell hypertrophy of bone marrow mesenchymal stem cells increase intramedullary cavity pressure, leading to osteonecrosis. By analyzing gene expression before and after adipogenic differentiation, we found that Microfibril-Associated Protein 5 (MFAP5) is significantly down-regulated in adipogenesis whilst the mechanism of MFAP5 in regulating the differentiation of bone marrow mesenchymal stem cells is unknown. The purpose of this study was to clarify the role of MAFP5 in adipogenesis and therefore provide a theoretical basis for future therapeutic options of osteonecrosis. By knockdown or overexpression of MFAP5 in C3H10 and 3T3-L1 cells, we found that MFAP5 was significantly down-regulated as a key regulator of adipogenic differentiation, and identified the underlying downstream molecular mechanism. MFAP5 directly bound to and inhibited the expression of Staphylococcal Nuclease And Tudor Domain Containing 1, an essential coactivator of PPARγ, exerting an important regulatory role in adipogenesis.

Figures
Products