Key result
Treatment with the endoplasmic reticulum stress inhibitor TUDCA significantly reduced ox-LDL-induced expression of osteogenic and ER stress markers (BMP2, PERK, ATF4, CHOP) in rabbit aortic valve interstitial cells.
Why the study?
Calcific aortic valve disease is a crucial component of degenerative valvular disease in aging populations, prompting investigation into the effect of endoplasmic reticulum stress on valvular osteogenesis.
Does TUDCA reduce ox-LDL-induced osteogenic transformation in rabbit aortic valve interstitial cells?
Does TUDCA reduce ox-LDL-induced osteogenic transformation in rabbit aortic valve interstitial cells?
p-value: p=<0.05
Inhibition of endoplasmic reticulum stress with TUDCA attenuates ox-LDL-induced osteogenic transformation in rabbit aortic valve interstitial cells.
TUDCA attenuates VIC osteogenesis in vitro; leaves open whether ER stress inhibition offers a therapeutic target in human CAVD.
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.
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Tao et al. (2022) studied Calcific Aortic Valve Disease (in vitro model) (n=8). TUDCA vs. ox-LDL alone was evaluated on Expression levels of BMP2, PERK, ATF4, and CHOP (p=<0.05). Treatment with the endoplasmic reticulum stress inhibitor TUDCA significantly reduced ox-LDL-induced expression of osteogenic and ER stress markers (BMP2, PERK, ATF4, CHOP) in rabbit aortic valve interstitial cells.
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