ArticleCell calcium2010
Store-operated Ca(2+) entry is not essential for PDGF-BB induced phenotype modulation in rat aortic smooth muscle.
Article in Cell calcium, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Characterization of PDGF-Induced Subcellular Calcium Regulation through Calcium Channels in Airway Smooth Muscle Cells by FRET Biosensors.Biosensors · 2024Article
- The right ventricular transcriptome signature in Ossabaw swine with cardiometabolic heart failure: implications for the coronary vasculature.Physiological genomics · 2021Article
- Chronic interval exercise training prevents BKJournal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Heart failure with preserved ejection fraction: chronic low-intensity interval exercise training preserves myocardial O2 balance and diastolic function.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Suppression of smooth muscle cell (SMC) differentiation marker genes is central to SMC phenotype modulation during vasculo-proliferative diseases such as atherosclerosis and restenosis. Upregulation of the intermediate-conductance Ca(2+)-activated K(+) channel (K(Ca)3.1) is integral for mitogen-induced suppression of SMC marker genes and post-angioplasty restenosis. Modulation of SMC marker gene expression has been observed following Ca(2+) influx from multiple sources, however, it is unknown whether upregulation of K(Ca)3.1 and/or suppression of SMC differentiation genes is dependent on a Ca(2+) mediated mechanism. The purpose of this study was to determine the dependence of mitogen-induced SMC phenotype modulation on store-operated Ca(2+) entry (SOCE). In growth-arrested, differentiated rat aortic SMCs, platelet-derived growth factor-BB (PDGF-BB) augmented SOCE. However, PDGF-BB induced upregulation of K(Ca)3.1 and downregulation of the SMC marker gene smooth muscle myosin heavy chain (SMMHC) and myocardin was not dependent on SOCE. Co-treatment with the iPLA2 inhibitor bromoenol lactone (BEL) inhibited the effects of PDGF-BB on SMC phenotype modulation and SOCE. Our results indicate SOCE is not required for PDGF-BB induced phenotype modulation in rat aortic SMCs. Rather, we implicate a novel BEL-sensitive mechanism which regulates both SOCE and phenotype modulation, independently.
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