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Inhibition of LSD1 phosphorylation alleviates colitis symptoms induced by dextran sulfate sodium
Chaeyoon Oh1, Jiyeong Jeong2,3, Se Kyu Oh4, Sung Hee Baek4, Keun Il Kim1,2,*
1Department of Biological Sciences and 2Research Institute of Women’s Health, Sookmyung Women's University,
3Division of Pulmonary and Critical Care Medicine, Seoul National University Hospital,
4Department of Biological Sciences, Seoul National University
Inflammatory Bowel Disease is caused by an acute or chronic dysfunction of the mucosal inflammatory system in the intestinal tract. In line with the results of our previous study, wherein we found that the PKCメ-LSD1-NF-リB signaling plays a critical role in the prolonged activation of the inflammatory response, we aimed to investigate the effect of signaling on colitis in the present study. Lsd1 S112A knock-in (Lsd1SA/SA) mice, harboring a deficiency in phosphorylation by PKCメ, exhibited less severe colitis symptoms and a relatively intact colonic epithelial lining in dextran sulfate sodium (DSS)-induced colitis models. Additionally, a reduction in pro-inflammatory gene expression and immune cell recruitment into damaged colon tissues in Lsd1SA/SA mice was observed upon DSS administration. Furthermore, LSD1 inhibition alleviated colitis symptoms and reduced colonic inflammatory responses. Both LSD1 phosphorylation and its activity jointly play a role in the progression of DSS-induced colitis. Therefore, the inhibition of LSD1 activity could potentially protect against the colonic inflammatory response.
Abstract, Accepted Manuscript(in press) [Submitted on November 29, 2019, Accepted on January 16, 2020]
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