Limits...
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

Levels of Cav1, TRPC1, and their complexes in gastric mucosa after hypertonic NaCl‐induced injury in mice. After cell lysates (500 μg) were immunoprecipitated (IP) by the specific Ab against TRPC1, precipitates were subjected to SDS‐PAGE (10% acrylamide). Levels of Cav1 and TRPC1 proteins were measured using western blot analysis with the antibody against Cav1 or TRPC1. Three separate experiments were performed that showed similar results.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4255804&req=5

fig03: Levels of Cav1, TRPC1, and their complexes in gastric mucosa after hypertonic NaCl‐induced injury in mice. After cell lysates (500 μg) were immunoprecipitated (IP) by the specific Ab against TRPC1, precipitates were subjected to SDS‐PAGE (10% acrylamide). Levels of Cav1 and TRPC1 proteins were measured using western blot analysis with the antibody against Cav1 or TRPC1. Three separate experiments were performed that showed similar results.

Mentions: Third, we examined the association of Cav1 with TRPC1 in the extracts of gastric mucosa during mucosal repair after hypertonic NaCl‐induced injury. As shown in Figure 3, Cav1/TRPC1 complexes as measured by IP with anti‐TRPC1 antibody increased significantly 6 h after the administration of hypertonic NaCl and this increase was continued until 16 h in control littermate mice. In contrast, Cav1/TRPC1 complex in the gastric mucosa was undetectable in Cav1−/− mice during repair after injury. These results clearly indicate that Cav1 plays a critical role in mucosal repair after injury through a process involving TRPC1.


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)

Levels of Cav1, TRPC1, and their complexes in gastric mucosa after hypertonic NaCl‐induced injury in mice. After cell lysates (500 μg) were immunoprecipitated (IP) by the specific Ab against TRPC1, precipitates were subjected to SDS‐PAGE (10% acrylamide). Levels of Cav1 and TRPC1 proteins were measured using western blot analysis with the antibody against Cav1 or TRPC1. 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

fig03: Levels of Cav1, TRPC1, and their complexes in gastric mucosa after hypertonic NaCl‐induced injury in mice. After cell lysates (500 μg) were immunoprecipitated (IP) by the specific Ab against TRPC1, precipitates were subjected to SDS‐PAGE (10% acrylamide). Levels of Cav1 and TRPC1 proteins were measured using western blot analysis with the antibody against Cav1 or TRPC1. Three separate experiments were performed that showed similar results.
Mentions: Third, we examined the association of Cav1 with TRPC1 in the extracts of gastric mucosa during mucosal repair after hypertonic NaCl‐induced injury. As shown in Figure 3, Cav1/TRPC1 complexes as measured by IP with anti‐TRPC1 antibody increased significantly 6 h after the administration of hypertonic NaCl and this increase was continued until 16 h in control littermate mice. In contrast, Cav1/TRPC1 complex in the gastric mucosa was undetectable in Cav1−/− mice during repair after injury. These results clearly indicate that Cav1 plays a critical role in mucosal repair after injury through a process involving TRPC1.

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