CARM1 regulates senescence during airway epithelial cell injury in COPD pathogenesis.

CARM1 regulates senescence during airway epithelial cell injury in COPD pathogenesis. Am J Physiol Lung Cell Mol Physiol. 2019 Aug 28;: Authors: Sarker RSJ, Conlon TM, Morrone C, Srivastava B, Konyalilar N, Verleden SE, Bayram H, Fehrenbach H, Yildirim AÖ Abstract Chronic obstructive pulmonary disease (COPD) is a life-threatening lung disease. Although cigarette smoke was considered the main cause of development, the heterogeneous nature of the disease leaves it unclear whether other factors contribute to the predisposition or impaired regeneration response observed. Recently, epigenetic modification has emerged to be a key player in the pathogenesis of COPD. The addition of methyl groups to arginine residues in both histone and non-histone proteins by protein arginine methyltransferases (PRMTs), is an important posttranslational epigenetic modification event regulating cellular proliferation, differentiation, apoptosis and senescence. Here, we hypothesize that coactivator-associated arginine methyltransferase-1 (CARM1) regulates airway epithelial cell injury in COPD pathogenesis by controlling cellular senescence. Using the naphthalene (NA)-induced mouse model of airway epithelial damage, we demonstrate that loss of CC10-positive club cells is accompanied by a reduction in CARM1 expressing cells of the airway epithelium. Furthermore, Carm1 haploinsuffficent mice showed perturbed club cell regeneration following NA-treatment. In add...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - Category: Cytology Authors: Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research