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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Liu, Haiyan Chen, Xi Liu, Guilin Xu, Guiliang Xiong, Sidong Zheng, Biao |
| Description | Author Affiliation: Xu G ( From the Jiangsu Key Laboratory of Infection and Immunity, Institute of Biological and Medical Sciences, Soochow University, Suzhou 215123, China.); Liu G ( From the Jiangsu Key Laboratory of Infection and Immunity, Institute of Biological and Medical Sciences, Soochow University, Suzhou 215123, China.); Xiong S ( From the Jiangsu Key Laboratory of Infection and Immunity, Institute of Biological and Medical Sciences, Soochow University, Suzhou 215123, China.); Liu H ( From the Jiangsu Key Laboratory of Infection and Immunity, Institute of Biological and Medical Sciences, Soochow University, Suzhou 215123, China.); Chen X ( the Shanghai Key Laboratory of Regulatory Biology, School of Biological Sciences, East China Normal University, Shanghai 200241, China, and the Department of Pathology and Immunology, Baylor College of Medicine, Houston, Texas 77030 xichen0919@gmail.com.); Zheng B ( the Shanghai Key Laboratory of Regulatory Biology, School of Biological Sciences, East China Normal University, Shanghai 200241, China, and the Department of Pathology and Immunology, Baylor College of Medicine, Houston, Texas 77030 bzheng@bcm.edu.) |
| Abstract | SET and MYND domain-containing 2 (Smyd2), a histone 3 lysine 4- and histone 3 lysine 36 (H3K36)-specific methyltransferase, plays critical roles in cardiac development and tumorigenesis. However, the role of Smyd2 in immunity and inflammation remains poorly understood. In this study, we report that Smyd2 is a novel negative regulator for macrophage activation and M1 polarization. Elevated Smyd2 expression suppresses the production of proinflammatory cytokines, including IL-6 and TNF, and inhibits the expression of important cell surface molecules, including major MHC-II and costimulatory molecules. Furthermore, macrophages with high Smyd2 expression inhibit Th-17 cell differentiation but promote regulatory T cell differentiation as a result of increased TGF-ß production and decreased IL-6 secretion. In macrophages, Smyd2 specifically facilitates H3K36 dimethylation at Tnf and Il6 promoters to suppress their transcription and inhibits NF-κB and ERK signaling. Therefore, our data demonstrate that epigenetic modification by Smyd2-mediated H3K36 dimethylation at Tnf and Il6 promoters plays an important role in the regulation of macrophage activation during inflammation. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 9 |
| Volume Number | 290 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2015-02-27 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Gene Expression Regulation Histone-Lysine N-Methyltransferase Genetics Interleukin-6 Macrophages Metabolism Tumor Necrosis Factor-alpha Animals Blotting, Western Cell Differentiation Cell Line Cells, Cultured Flow Cytometry Histones Lysine MAP Kinase Signaling System Macrophage Activation Cytology Methylation Mice, Inbred C57BL Mutation NF-kappa B RNA Interference Reverse Transcriptase Polymerase Chain Reaction T-Lymphocytes, Regulatory Th17 Cells Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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