ArticlePhysiological reports2014
Caveolin-1 enhances rapid mucosal restitution by activating TRPC1-mediated Ca2+ signaling.
Article in Physiological reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
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- Endoplasmic Reticulum-Plasma Membrane Contact Sites as an Organizing Principle for Compartmentalized Calcium and cAMP Signaling.International journal of molecular sciences · 2021Review
- TheInternational journal of molecular sciences · 2021Article
- miR-222 represses expression of zipcode binding protein-1 and phospholipase C-γ1 in intestinal epithelial cells.American journal of physiology. Cell physiology · 2019Article
- Inhibition of Polyamine Biosynthesis Reverses CaCancers · 2019Article
- β-PIX plays an important role in regulation of intestinal epithelial restitution by interacting with GIT1 and Rac1 after wounding.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- c-Jun enhances intestinal epithelial restitution after wounding by increasing phospholipase C-γ1 transcription.American journal of physiology. Cell physiology · 2017Article
- Posttranscriptional regulation of 14-3-3ζ by RNA-binding protein HuR modulating intestinal epithelial restitution after wounding.Physiological reports · 2016Article
- Caveolin-1 overexpression in benign and malignant salivary gland tumors.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- RhoA enhances store-operated Ca2+ entry and intestinal epithelial restitution by interacting with TRPC1 after wounding.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Early rapid mucosal restitution occurs as a consequence of epithelial cell migration to reseal superficial wounds, a process independent of cell proliferation. Our previous studies revealed that the canonical transient receptor potential-1 (TRPC1) functions as a store-operated Ca(2+) channel (SOCs) in intestinal epithelial cells (IECs) and regulates epithelial restitution after wounding, but the exact mechanism underlying TRPC1 activation remains elusive. Caveolin-1 (Cav1) is a major component protein that is associated with caveolar lipid rafts in the plasma membrane and was recently identified as a regulator of store-operated Ca(2+) entry (SOCE). Here, we showed that Cav1 plays an important role in the regulation of mucosal restitution by activating TRPC1-mediated Ca(2+) signaling. Target deletion of Cav1 delayed gastric mucosal repair after exposure to hypertonic NaCl in mice, although it did not affect total levels of TRPC1 protein. In cultured IECs, Cav1 directly interacted with TRPC1 and formed Cav1/TRPC1 complex as measured by immunoprecipitation assays. Cav1 silencing in stable TRPC1-transfected cells by transfection with siCav1 reduced SOCE without effect on the level of resting [Ca(2+)]cyt. Inhibition of Cav1 expression by siCav1 and subsequent decrease in Ca(2+) influx repressed epithelial restitution, as indicated by a decrease in cell migration over the wounded area, whereas stable ectopic overexpression of Cav1 increased Cav1/TRPC1 complex, induced SOCE, and enhanced cell migration after wounding. These results indicate that Cav1 physically interacts with and activates TRPC1, thus stimulating TRPC1-mediated Ca(2+) signaling and rapid mucosal restitution after injury.
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