{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tsoyi K"],"funding":["National Institute of Arthritis and Musculoskeletal and Skin Diseases","NHLBI NIH HHS","National Heart, Lung, and Blood Institute","NIAMS NIH HHS"],"pagination":["2847"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8857282"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(1)"],"pubmed_abstract":["Rheumatoid arthritis (RA)-associated interstitial lung disease (RA-ILD) is the most common pulmonary complication of RA, increasing morbidity and mortality. Anti-citrullinated protein antibodies have been associated with the development and progression of both RA and fibrotic lung disease; however, the role of protein citrullination in RA-ILD remains unclear. Here, we demonstrate that the expression of peptidylarginine deiminase 2 (PAD2), an enzyme that catalyzes protein citrullination, is increased in lung homogenates from subjects with RA-ILD and their lung fibroblasts. Chemical inhibition or genetic knockdown of PAD2 in RA-ILD fibroblasts attenuated their activation, marked by decreased myofibroblast differentiation, gel contraction, and extracellular matrix gene expression. Treatment o"],"journal":["Scientific reports"],"pubmed_title":["Syndecan-2 regulates PAD2 to exert antifibrotic effects on RA-ILD fibroblasts."],"pmcid":["PMC8857282"],"funding_grant_id":["F32 HL151132","R01 AR070171","L30 HL149048","K01 AR074558","P01 HL114501"],"pubmed_authors":["Romero F","Xiong K","Ryter SW","El-Chemaly SY","Rosas IO","Liang X","Sun B","Chu SG","Beeton C","Cardenas R","Esposito AJ","Poli F","Bowen RG","Doyle TJ","Perrella MA","Tsoyi K","Ho IC","Celada LJ","Robertson MJ"],"additional_accession":[]},"is_claimable":false,"name":"Syndecan-2 regulates PAD2 to exert antifibrotic effects on RA-ILD fibroblasts.","description":"Rheumatoid arthritis (RA)-associated interstitial lung disease (RA-ILD) is the most common pulmonary complication of RA, increasing morbidity and mortality. Anti-citrullinated protein antibodies have been associated with the development and progression of both RA and fibrotic lung disease; however, the role of protein citrullination in RA-ILD remains unclear. Here, we demonstrate that the expression of peptidylarginine deiminase 2 (PAD2), an enzyme that catalyzes protein citrullination, is increased in lung homogenates from subjects with RA-ILD and their lung fibroblasts. Chemical inhibition or genetic knockdown of PAD2 in RA-ILD fibroblasts attenuated their activation, marked by decreased myofibroblast differentiation, gel contraction, and extracellular matrix gene expression. Treatment o","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2025-04-22T10:01:40.854Z","creation":"2025-04-05T23:22:37.415Z"},"accession":"S-EPMC8857282","cross_references":{"pubmed":["35181688"],"doi":["10.1038/s41598-022-06678-7"]}}