ArticleAmerican journal of physiology. Cell physiology2008
Rac1 promotes intestinal epithelial restitution by increasing Ca2+ influx through interaction with phospholipase C-(gamma)1 after wounding.
Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
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- Spermine protects intestinal barrier integrity through ras-related C3 botulinum toxin substrate 1/phospholipase C-γ1 signaling pathway in piglets.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2022Article
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- Colchicine protects against cartilage degeneration by inhibiting MMP13 expression via PLC-γ1 phosphorylation.Osteoarthritis and cartilage · 2021Article
- TRPC1-mediated CaPhysiological reports · 2021Article
- Review
- Microbial Metabolites Determine Host Health and the Status of Some Diseases.International journal of molecular sciences · 2019Review
- miR-222 represses expression of zipcode binding protein-1 and phospholipase C-γ1 in intestinal epithelial cells.American journal of physiology. Cell physiology · 2019Article
- Cell injury triggers actin polymerization to initiate epithelial restitution.Journal of cell science · 2018Article
- 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
- 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
- Caveolin-1 enhances rapid mucosal restitution by activating TRPC1-mediated Ca2+ signaling.Physiological reports · 2014Article
- Src-mediated caveolin-1 phosphorylation regulates intestinal epithelial restitution by altering Ca(2+) influx after wounding.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- UDP induces intestinal epithelial migration via the P2Y6 receptor.British journal of pharmacology · 2013Article
- Enterocyte loss of polarity and gut wound healing rely upon the F-actin-severing function of villin.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Polyamines regulate intestinal epithelial restitution through TRPC1-mediated Ca²+ signaling by differentially modulating STIM1 and STIM2.American journal of physiology. Cell physiology · 2012Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Intestinal mucosal restitution occurs as a consequence of epithelial cell migration and reseals superficial wounds after injury. This rapid reepithelialization is mediated in part by a phospholipase C-gamma1 (PLC-gamma1)-induced Ca(2+) signaling, but the exact mechanism underlying such signaling and its regulation remains elusive. The small GTP-binding protein Rac1 functions as a pivotal regulator of several signaling networks and plays an important role in regulating cell motility. The current study tests the hypothesis that Rac1 modulates intestinal epithelial cell migration after wounding by altering PLC-gamma1-induced Ca(2+) signaling. Inhibition of Rac1 activity by treatment with its inhibitor NSC-23766 or Rac1 silencing with small interfering RNA decreased store depletion-induced Ca(2+) influx and suppressed cell migration during restitution, whereas ectopic overexpression of Rac1 increased Ca(2+) influx and promoted cell migration. Rac1 physically interacted with PLC-gamma1 and formed Rac1/PLC-gamma1 complex in intestinal epithelial cells. PLC-gamma1 silencing in cells overexpressing Rac1 prevented stimulation of store depletion-induced Ca(2+) influx and cell migration after wounding. Polyamine depletion inhibited expression of both Rac1 and PLC-gamma1, decreased Rac1/PLC-gamma1 complex levels, reduced Ca(2+) influx, and repressed cell migration. Overexpression of Rac1 alone failed to rescue Ca(2+) influx after store depletion and cell migration in polyamine-deficient cells, because it did not alter PLC-gamma1 levels. These results indicate that Rac1 promotes intestinal epithelial cell migration after wounding by increasing Ca(2+) influx as a result of its interaction with PLC-gamma1.
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