ArticleJournal of cellular and molecular medicine2009
TRPC1 is regulated by caveolin-1 and is involved in oxidized LDL-induced apoptosis of vascular smooth muscle cells.
Article in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
- The effects of colchicine on lipoprotein(a)- and oxidized phospholipid-associated cardiovascular disease risk.European journal of preventive cardiology · 2025Trial
- Oxysterol-Induced Inflammation in Human Diseases: Strategies for Treatment with Natural Compounds and Synthetic Molecules.Molecules (Basel, Switzerland) · 2025Review
- Gene expression patterns of the LDL receptor and its inhibitor Pcsk9 in the adult zebrafish brain suggest a possible role in neurogenesis.The European journal of neuroscience · 2025Article
- Transient receptor potential channels as key regulators of cell death in atherosclerosis.Frontiers in immunology · 2025Review
- Advanced age and female sex protect cerebral arteries from mitochondrial depolarization and apoptosis during acute oxidative stress.Aging cell · 2024Article
- Mechanosensing and Mechanosignal Transduction in Atherosclerosis.Current atherosclerosis reports · 2023Review
- Role of mechanosensitive channels/receptors in atherosclerosis.American journal of physiology. Cell physiology · 2022Review
- Antioxidant and Cytoprotective Properties of Polyphenol-Rich Extracts fromAntioxidants (Basel, Switzerland) · 2021Article
- Role of Store-Operated CaBiomolecules · 2021Review
- Review
- TRPC and TRPV Channels' Role in Vascular Remodeling and Disease.International journal of molecular sciences · 2020Review
- Female sex and Western-style diet protect mouse resistance arteries during acute oxidative stress.American journal of physiology. Cell physiology · 2020Article
- Ion Channels in Pulmonary Hypertension: A Therapeutic Interest?International journal of molecular sciences · 2018Review
- Mouse models of atherosclerosis: a historical perspective and recent advances.Lipids in health and disease · 2017Review
- Store-operated calcium entry-activated autophagy protects EPC proliferation via the CAMKK2-MTOR pathway in ox-LDL exposure.Autophagy · 2017Article
- Loss of Epithelial Membrane Protein 2 Aggravates Podocyte Injury via Upregulation of Caveolin-1.Journal of the American Society of Nephrology : JASN · 2016Article
- Cardiac Mechano-Gated Ion Channels and Arrhythmias.Circulation research · 2016Review
- Role of protein kinase C δ in ER stress and apoptosis induced by oxidized LDL in human vascular smooth muscle cells.Cell death & disease · 2013Article
- Ceramide mediates Ox-LDL-induced human vascular smooth muscle cell calcification via p38 mitogen-activated protein kinase signaling.PloS one · 2013Article
- Cytoskeletal regulation of TRPC channels in the cardiorenal system.Current hypertension reports · 2012Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidized low-density lipoprotein (oxLDL) induced-apoptosis of vascular cells may participate in plaque instability and rupture. We have previously shown that vascular smooth muscle cells (VSMC) stably expressing caveolin-1 were more susceptible to oxLDL-induced apoptosis than VSMC expressing lower level of caveolin-1, and this was correlated with enhanced Ca(2+) entry and pro-apoptotic events. In this study, we aimed to identify the molecular events involved in oxLDL-induced Ca(2+) influx and their regulation by the structural protein caveolin-1. In VSMC, transient receptor potential canonical-1 (TRPC1) silencing by ARN interference prevents the Ca(2+) influx and reduces the toxicity induced by oxLDL. Moreover, caveolin-1 silencing induces concomitant decrease of TRPC1 expression and reduces oxLDL-induced apoptosis of VSMC. OxLDL enhanced the cell surface expression of TRPC1, as shown by biotinylation of cell surface proteins, and induced TRPC1 translocation into caveolar compartment, as assessed by subcellular fractionation. OxLDL-induced TRPC1 translocation was dependent on actin cytoskeleton and associated with a dramatic rise of 7-ketocholesterol (a major oxysterol in oxLDL) into caveolar membranes, whereas the caveolar content of cholesterol was unchanged. Altogether, the reported results show that TRPC1 channels play a role in Ca(2+) influx and Ca(2+) homeostasis deregulation that mediate apoptosis induced by oxLDL. These data also shed new light on the role of caveolin-1 and caveolar compartment as important regulators of TRPC1 trafficking to the plasma membrane and apoptotic processes that play a major role in atherosclerosis.
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Registered trials
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