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Caveolin-1 enhances rapid mucosal restitution by activating TRPC1-mediated Ca2+ signaling.

Rathor N, Chung HK, Wang SR, Wang JY, Turner DJ, Rao JN - Physiol Rep (2014)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery, Cell Biology Group, University of Maryland School of Medicine, Baltimore, Maryland, USA Baltimore VA Medical Center, Baltimore, Maryland, USA.

No MeSH data available.


Related in: MedlinePlus

Cav1 and TRPC1 protein expression in gastric mucosa isolated from Cav1−/− mice and control wild‐type littermates. Levels of Cav1 and TRPC1 were examined by western blot analysis. Actin immunoblotting was performed as an internal control for equal loading. Three separate experiments were performed that showed similar results.
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fig01: Cav1 and TRPC1 protein expression in gastric mucosa isolated from Cav1−/− mice and control wild‐type littermates. Levels of Cav1 and TRPC1 were examined by western blot analysis. Actin immunoblotting was performed as an internal control for equal loading. Three separate experiments were performed that showed similar results.

Mentions: To determine the in vivo function of Cav1 in the regulation of gut mucosal restitution, Cav1−/− mice were used in this study. First, we characterized Cav1−/− mice to verify the basal levels of Cav1 and TRPC1 proteins in the gastric mucosa. Heterozygous Cav1+/− mice appeared phenotypically normal and were subsequently intercrossed for the generation of homozygous Cav1−/− mice. Generally, Cav1−/− mice looked normal; there were no significant differences in body weight, gastrointestinal gross morphology, and general appearances between Cav1−/− mice and littermate controls (data not shown). Age‐matched Cav1−/− mice and littermate control mice (3 months old) were used for phenotype analysis. Mucosal scrapings were isolated and analyzed by western immunoblotting assays using specific anti‐Cav1 or TRPC1 antibody. As shown in Figure 1, gastric mucosa expressed a very high basal level of Cav1 protein in control wild‐type littermates, but Cav1 protein was undetectable in the mucosa in Cav1−/− mice, as expected. However, there were no significant changes in basal levels of TRPC1 expression in the gastric mucosa between control littermate and Cav1−/− mice.


Caveolin-1 enhances rapid mucosal restitution by activating TRPC1-mediated Ca2+ signaling.

Rathor N, Chung HK, Wang SR, Wang JY, Turner DJ, Rao JN - Physiol Rep (2014)

Cav1 and TRPC1 protein expression in gastric mucosa isolated from Cav1−/− mice and control wild‐type littermates. Levels of Cav1 and TRPC1 were examined by western blot analysis. Actin immunoblotting was performed as an internal control for equal loading. Three separate experiments were performed that showed similar results.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255804&req=5

fig01: Cav1 and TRPC1 protein expression in gastric mucosa isolated from Cav1−/− mice and control wild‐type littermates. Levels of Cav1 and TRPC1 were examined by western blot analysis. Actin immunoblotting was performed as an internal control for equal loading. Three separate experiments were performed that showed similar results.
Mentions: To determine the in vivo function of Cav1 in the regulation of gut mucosal restitution, Cav1−/− mice were used in this study. First, we characterized Cav1−/− mice to verify the basal levels of Cav1 and TRPC1 proteins in the gastric mucosa. Heterozygous Cav1+/− mice appeared phenotypically normal and were subsequently intercrossed for the generation of homozygous Cav1−/− mice. Generally, Cav1−/− mice looked normal; there were no significant differences in body weight, gastrointestinal gross morphology, and general appearances between Cav1−/− mice and littermate controls (data not shown). Age‐matched Cav1−/− mice and littermate control mice (3 months old) were used for phenotype analysis. Mucosal scrapings were isolated and analyzed by western immunoblotting assays using specific anti‐Cav1 or TRPC1 antibody. As shown in Figure 1, gastric mucosa expressed a very high basal level of Cav1 protein in control wild‐type littermates, but Cav1 protein was undetectable in the mucosa in Cav1−/− mice, as expected. However, there were no significant changes in basal levels of TRPC1 expression in the gastric mucosa between control littermate and Cav1−/− mice.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery, Cell Biology Group, University of Maryland School of Medicine, Baltimore, Maryland, USA Baltimore VA Medical Center, Baltimore, Maryland, USA.

No MeSH data available.


Related in: MedlinePlus