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MEF2C regulates osteoclastogenesis and pathologic bone resorption via c-FOS

bone Research 2021年第1期9卷 50-62页

作者： Takayuki Fujii Koichi Murata Se-Hwan Mun Seyeon bae Ye Ji Lee Tannia Pannellini Kyuho Kang David Oliver Kyung-Hyun Park-Min lionel b.ivashkiv Arthritis and Tissue Degeneration Program and David Z.Rosensweig Genomics Research Center Hospital for Special SurgeryNew YorkNY 10021USA Department of Orthopaedic Surgery Kyoto University Graduate School of MedicineSakyoKyoto 606-8507Japan Department of Advanced Medicine for Rheumatic Diseases Kyoto University Graduate School of MedicineSakyoKyoto 606-8507Japan Department of biology Chungbuk National UniversityCheongju 28644Republic of Korea bCMb Allied Program Weill Cornell Graduate School of Medical ScienceNew YorkNY 10021USA Immunology and Microbial Pathogenesis Program Weill Cornell Graduate School of Medical ScienceNew YorkNY 10021USA

Osteoporosis is a metabolic bone disease with dysregulated coupling between bone resorption and bone formation,which results in decreased bone mineral *** MEF2C locus,which encodes the transcription factor MADS box transcription enhancer factor 2,polypeptide C(MEF2C),is strongly associated with adult osteoporosis and osteoporotic *** the role of MEF2C in bone and cartilage formation by osteoblasts,osteocytes,and chondrocytes has been studied,the role of MEF2C in osteoclasts,which mediate bone resorption,remains *** this study,we identified MEF2C as a positive regulator of human and mouse osteoclast *** decreased MEF2C expression resulted in diminished osteoclastogenesis,ectopic expression of MEF2C enhanced osteoclast *** transcriptomic and bioinformatic approaches,we found that MEF2C promotes the RANKL-mediated induction of the transcription factors c-FOS and NFATc1,which play a key role in ***,MEF2C binds to FOS regulatory regions to induce c-FOS expression,leading to the activation of NFATC1 and downstream *** deletion of Mef2c in mice resulted in increased bone mass under physiological conditions and protected mice from bone erosion by diminishing osteoclast formation in K/bxN serum induced arthritis,a murine model of inflammatory *** findings reveal direct regulation of osteoclasts by MEF2C,thus adding osteoclasts as a cell type in which altered MEF2C expression or function can contribute to pathological bone remodeling.

关键词： osteoclast MEF2C pathologic

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RbP-J is required for M2 macrophage polarization in response to chitin and mediates expression of a subset of M2 genes

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Protein & Cell 2016年第3期7卷 201-209页

作者： Julia Foldi Yingli Shang baohong Zhao lionel b. ivashkiv Xiaoyu Hu Graduate Program in Immunology and Microbial Pathogenesis Weill Cornell Graduate School of Medical Sciences New York NY 10021 USA School of Medicine and Institute for Immunology Tsinghua University Beijing 100084 China Arthritis and Tissue Degeneration Program Hospital for Special Surgery New York NY 10021 USA

Development of alternatively activated （M2） macrophage phenotypes is a complex process that is coordinately regulated by a plethora of pathways and factors. Here, we report that RbP-J, a DNA-binding protein that integrates signals from multiple pathways including the Notch pathway, is critically involved in polarization of M2 macrophages. Mice deficient in RbP-J in the myeloid compartment exhibited impaired M2 phenotypes in vivo in a chitin-induced model of M2 polarization. Consistent with the in vivo findings, M2 polarization was partially compromised in vitro in Rbpj-deficient macrophages as demonstrated by reduced expression of a subset of M2 effector molecules including arginase 1. Functionally, myeloid Rbpj deficiency impaired M2 effector functions including recruitment of eosinophils and suppression of T cell proliferation. Collectively, we have identified RbP- Jas an essential regulator of differentiation and function of alternatively activated macrophages.

关键词： macrophages RbP-J M2 arginase chitin

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