PMID- 35355558 OWN - NLM STAT- MEDLINE DCOM- 20220401 LR - 20220520 IS - 1664-2392 (Print) IS - 1664-2392 (Electronic) IS - 1664-2392 (Linking) VI - 13 DP - 2022 TI - Mechanism of Endoplasmic Reticulum Stress Pathway in the Osteogenic Phenotypic Transformation of Aortic Valve Interstitial Cells. PG - 856331 LID - 10.3389/fendo.2022.856331 [doi] LID - 856331 AB - BACKGROUND AND PURPOSE: Calcific Aortic Valve Disease (CAVD) is a crucial component of degenerative valvular disease in old age and with the increasing prevalence of the aging population. we hope that by modeling valvular osteogenesis and intervening with endoplasmic reticulum stress inhibitor TUDCA to observe the effect of endoplasmic reticulum stress on valve osteogenesis. METHODS: In this study, rabbit heart valvular interstitial cells (VICs) were isolated and cultured. They treated with ox-LDL (Oxidized Low Density Lipoprotein) stimulation to establish a model of valvular osteogenic transformation. BMP2 (Bone Morphogenetic Protein 2), PERK (Protein kinase R-like endoplasmic reticulum kinase), CHOP (CCAAT/enhancer-binding protein homologous protein) and transcriptional regulatory factor ATF4 (Activating Transcription Factor 4 )were recorded after intervention with ER stress inhibitor TUDCA. The effects of er stress on valvular osteogenic transformation were analyzed. RESULT: After stimulation of VICs with ox-LDL, the expression levels of BMP2, PERK, CHOP, and ATF4 increased. However, TUDCA treatment can alleviate the increased expression levels of BMP2, PERK ATF4, and CHOP under ox-LDL stimulation to a certain extent. CONCLUSION: The endoplasmic reticulum stress signaling pathway is involved in ox-LDL-induced calcification of rabbit valve interstitial cells. Inhibition of endoplasmic reticulum stress using TUDCA can improve the progression of rabbit aortic valve calcification. CI - Copyright (c) 2022 Tao, Geng, Dang, Xu, Zhao, Zou and Li. FAU - Tao, Yiming AU - Tao Y AD - Department of Intensive Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. AD - The Emergency Department, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. FAU - Geng, Yimin AU - Geng Y AD - Department of Intensive Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. AD - The Emergency Department, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. FAU - Dang, Wenpei AU - Dang W AD - Department of Intensive Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. AD - The Emergency Department, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. FAU - Xu, Xinxin AU - Xu X AD - Department of Intensive Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. AD - The Emergency Department, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. FAU - Zhao, Hui AU - Zhao H AD - Department of Intensive Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. AD - The Emergency Department, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. FAU - Zou, Lijuan AU - Zou L AD - Department of Intensive Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. AD - The Emergency Department, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. FAU - Li, Yongsheng AU - Li Y AD - Department of Intensive Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. AD - The Emergency Department, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. LA - eng PT - Journal Article DEP - 20220308 PL - Switzerland TA - Front Endocrinol (Lausanne) JT - Frontiers in endocrinology JID - 101555782 SB - IM MH - Animals MH - Aortic Valve/metabolism MH - *Aortic Valve Stenosis/metabolism MH - *Calcinosis MH - Cells, Cultured MH - Endoplasmic Reticulum Stress MH - Osteogenesis MH - Rabbits PMC - PMC8959129 OTO - NOTNLM OT - BMP2 OT - TUDCA OT - aortic valve calcification OT - endoplasmic reticulum stress OT - ox-LDL OT - valve interstitial cells COIS- The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. EDAT- 2022/04/01 06:00 MHDA- 2022/04/02 06:00 PMCR- 2022/01/01 CRDT- 2022/03/31 05:18 PHST- 2022/01/17 00:00 [received] PHST- 2022/02/07 00:00 [accepted] PHST- 2022/03/31 05:18 [entrez] PHST- 2022/04/01 06:00 [pubmed] PHST- 2022/04/02 06:00 [medline] PHST- 2022/01/01 00:00 [pmc-release] AID - 10.3389/fendo.2022.856331 [doi] PST - epublish SO - Front Endocrinol (Lausanne). 2022 Mar 8;13:856331. doi: 10.3389/fendo.2022.856331. eCollection 2022.