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LSD1-S112A exacerbates the pathogenesis of CSE/LPS-induced chronic obstructive pulmonary disease in mice
Jiyeong Jeong1,2 (Post-doc), Chaeyoon Oh3 (Graduate student), Jiwon Kim3 (Graduate student), Chul-Gyu Yoo2 (Professor), Keun Il Kim 1,3,* (Professor)
1Research Institute of Women’s Health, Sookmyung Women’s University,
2Internal Medicine, Seoul National University College of Medicine,
3Biological Sciences, Sookmyung Women’s University
Lysine-specific demethylase 1 (LSD1) is an epigenetic regulator that modulates the chromatin status, contributing to gene activation or repression. The post-translational modification of LSD1 is critical for the regulation of many of its biological processes. Phosphorylation of serine 112 of LSD1 by protein kinase C alpha (PKCメ) is crucial for regulating inflammation, but its physiological significance is not fully understood. This study aimed to investigate the role of LSD1-S112A, a phosphorylation defective mutant, in the cigarette smoke extract (CSE)/lipopolysaccharide (LPS)-induced chronic obstructive pulmonary disease COPD model using Lsd1SA/SA mice and to explore the potential mechanism underpinning the development of COPD. We found that Lsd1SA/SA mice exhibited increased susceptibility to CSE/LPS-induced COPD, including high inflammatory cell influx into the bronchoalveolar lavage fluid and airspace enlargement. Additionally, the higher gene expression associated with the inflammatory response and oxidative stress was observed in cells and mice containing LSD1-S112A. Similar results were obtained from the mouse embryonic fibroblasts exposed to a PKCメ inhibitor, Go6976. Thus, the lack of LSD1 phosphorylation exacerbates CSE/LPS-induced COPD by elevating inflammation and oxidative stress.
Abstract, Accepted Manuscript(in press) [Submitted on March 4, 2021, Accepted on May 25, 2021]
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