ArticleThe Biochemical journal2006
Induced TRPC1 expression sensitizes intestinal epithelial cells to apoptosis by inhibiting NF-kappaB activation through Ca2+ influx.
Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 83 citations in OpenAlex.
- Dopaminergic neurotoxins induce cell death by attenuating NF-κB-mediated regulation of TRPC1 expression and autophagy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Role of TRP ion channels in cancer and tumorigenesis.Seminars in immunopathology · 2016Review
- Article
- Carvacrol together with TRPC1 elimination improve functional recovery after traumatic brain injury in mice.Journal of neurotrauma · 2012Article
- Distinct regulation of cytoplasmic calcium signals and cell death pathways by different plasma membrane calcium ATPase isoforms in MDA-MB-231 breast cancer cells.The Journal of biological chemistry · 2012Article
- Induced expression of STIM1 sensitizes intestinal epithelial cells to apoptosis by modulating store-operated Ca2+ influx.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2012Article
- Polyamines and Gut Mucosal Homeostasis.Journal of gastrointestinal & digestive system · 2012Article
- Article
- Transient receptor potential (TRP) channels as drug targets for diseases of the digestive system.Pharmacology & therapeutics · 2011Review
- Molecular mechanisms underlying Ca2+-mediated motility of human pancreatic duct cells.American journal of physiology. Cell physiology · 2010Article
- STIM1 translocation to the plasma membrane enhances intestinal epithelial restitution by inducing TRPC1-mediated Ca2+ signaling after wounding.American journal of physiology. Cell physiology · 2010Article
- Cellular functions of transient receptor potential channels.The international journal of biochemistry & cell biology · 2010Review
- Molecular and functional characterization of non voltage-operated Ca entry in gastrointestinal neuroendocrine tumor cells.International journal of physiology, pathophysiology and pharmacology · 2010Article
- Do calcium channel blockers rescue dying photoreceptors in the Pde6b ( rd1 ) mouse?Advances in experimental medicine and biology · 2010Review
- TRPC1 is regulated by caveolin-1 and is involved in oxidized LDL-induced apoptosis of vascular smooth muscle cells.Journal of cellular and molecular medicine · 2009Article
- A functional single-nucleotide polymorphism in the TRPC6 gene promoter associated with idiopathic pulmonary arterial hypertension.Circulation · 2009Article
- Physiology and pathophysiology of canonical transient receptor potential channels.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Review
- Deoxycholyltaurine rescues human colon cancer cells from apoptosis by activating EGFR-dependent PI3K/Akt signaling.Journal of cellular physiology · 2008Article
- Overexpression of TRPC3 increases apoptosis but not necrosis in response to ischemia-reperfusion in adult mouse cardiomyocytes.American journal of physiology. Cell physiology · 2008Article
- Restricted epithelial proliferation by lacritin via PKCalpha-dependent NFAT and mTOR pathways.The Journal of cell biology · 2006Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Apoptosis occurs within crypts and at the intestinal luminal surface and plays a critical role in mucosal homoeostasis. NF-kappaB (nuclear factor-kappaB) is the central regulator of the transcription of genes involved in apoptosis, and its activity is highly regulated in the intestinal mucosa. We have recently demonstrated that TRPC1 (transient receptor potential canonical-1) is expressed in IECs (intestinal epithelial cells) and functions as a Ca2+ permeable channel activated by Ca2+ store depletion. The present study tests the hypothesis that TRPC1 channels are implicated in the regulation of apoptosis by inhibiting NF-kappaB through the induction of TRPC1-mediated Ca2+ influx in the IEC-6 line. The expression of TRPC1 induced by stable transfection of IEC-6 cells with the wild-type TRPC1 gene (IEC-TRPC1 cells) increased Ca2+ influx after Ca2+ store depletion and repressed NF-kappaB transactivation, which was associated with an increase in susceptibility to apoptosis induced by exposure to TNFalpha (tumour necrosis factor-alpha) plus CHX (cycloheximide) (TNF-alpha/CHX), or STS (staurosporine). By contrast, the induction of endogenous NF-kappaB activity, by the depletion of cellular polyamines, promoted resistance to apoptosis, which was prevented by the ectopic expression of the IkappaBalpha super-repressor. Furthermore, inhibition of TRPC1 expression by transfection with siRNA (small interfering RNA) targeting TRPC1 (siTRPC1) decreased Ca2+ influx, increased NF-kappaB transactivation, and prevented the increased susceptibility of IEC-TRPC1 cells to apoptosis. Decreasing Ca2+ influx by exposure to a Ca2+-free medium also induced NF-kappaB activity and blocked the increased susceptibility to apoptosis of stable IEC-TRPC1 cells. These results indicate that induced TRPC1 expression sensitizes IECs to apoptosis by inhibiting NF-kappaB activity as a result of the stimulation of Ca2+ influx.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.