MYSM1/miR-150/FLT3 inhibits B1a cell proliferation
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Xiao-Xia Jiang1,*, Yu Liu1,2,*, Hong Li1,*, Yaping Gao1, Rong Mu2, Jianping Guo2, Jing Zhang2, Yan-Mei Yang1, Fengjun Xiao3, Bing Liu4, Changyong Wang1, Beifen Shen1,6, Si-Yi Chen5, Zhanguo Li2, Guang Yang1,6
1Beijing Institute of Basic Medical Sciences, Beijing, China
2Department of Rheumatology and Immunology, People’s Hospital, Peking University, Beijing, China
3Institute of Radiation Medicine, Beijing, China
4307-Ivy Translational Medicine Center, Laboratory of Oncology, Affiliated Hospital of Academy of Military Medical Sciences, Beijing, China
5Department of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
6State Key Laboratory of Toxicology and Medical Countermeasures, Beijing Institute of Pharmacology and Toxicology, Beijing, China
*These authors contributed equally to this work
Guang Yang, email: [email protected]
Zhanguo Li, email: [email protected]
Si-Yi Chen, email: [email protected]
Keywords: MYSM1, miR-150, FLT3, B1a, proliferation
Received: June 06, 2016 Accepted: August 25, 2016 Published: August 31, 2016
The aberrant expansion of B1a cells has been observed in several murine autoimmune disease models; however, the mechanism of such proliferation of B1a cells is still limited. Here, we identify that Myb Like, SWIRM And MPN Domains 1 (MYSM1), a histone H2A deubiquitinase, plays an intrinsic role in the proliferation of B1a cells where MYSM1 deficiency results in the increased proliferation of B1a cells in mice. We demonstrate that MYSM1 recruits c-Myc to the promoter of miR-150 and stimulates the transcription of miR-150. Our further investigation shows that miR-150 decreases FMS-like tyrosine kinase 3 (FLT3) in B1a cells. In agreement with our animal studies, the percentage of FLT3+ B1 cells in Systemic Lupus Erythematosus (SLE) patients is significantly higher than healthy control. Thus, this study uncovers a novel pathway MYSM1/miR-150/FLT3 that inhibits proliferation of B1a, which may be involved in the pathogenesis of SLE.
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