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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

Histological appearance and macroscopic damage of gastric mucosa after exposure to hypertonic NaCl in mice. Gastric mucosal injury was induced by intragastric administration of 3.4 mol/L NaCl as described in Material and Methods section. Mice were euthanized during recovery from injury at 0, 3, 6, and 16 h after the administration of NaCl. (A) Paraffin‐embedded sections with H/E staining from different times after injury. Scale bar, 100 μm. Original magnification ×100. (B) Ulcer index in gastric mucosa after injury. Values are means ± SEM from four to five mice/group. *P < 0.05 compared with control littermates.
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fig02: Histological appearance and macroscopic damage of gastric mucosa after exposure to hypertonic NaCl in mice. Gastric mucosal injury was induced by intragastric administration of 3.4 mol/L NaCl as described in Material and Methods section. Mice were euthanized during recovery from injury at 0, 3, 6, and 16 h after the administration of NaCl. (A) Paraffin‐embedded sections with H/E staining from different times after injury. Scale bar, 100 μm. Original magnification ×100. (B) Ulcer index in gastric mucosa after injury. Values are means ± SEM from four to five mice/group. *P < 0.05 compared with control littermates.

Mentions: Second, we examined changes in the rate of gastric mucosal repair and the levels of Cav1/TRPC1 complexes in the mucosal tissue after exposure to hypertonic NaCl as described previously (Coimbra et al. 1997; Tatemichi et al. 2003). Exposure of the gastric mucosa to 3.4 mol/L NaCl induced visible lesions in littermate and Cav1−/− mice. Histological examination (Fig. 2A) and macroscopic damage (Fig. 2B) showed that the maximal mucosal injury occurred 3 h after intragastric administration of hypertonic NaCl and that the repair process began 6 h and was almost completed 16 h in littermate mice. However, target deletion of the Cav1 gene significantly delayed gastric mucosal repair of hypertonic NaCl‐induced injury. We have also examined changes in mucosal injury at 1 and 2 h after the exposure to NaCl and found no significant damage to gastric mucosa (data not shown). At 16 h after administration of hypertonic NaCl, visible lesions in the gastric mucosa were still noticeable in Cav1−/− mice (Fig. 2Ab, right panel), indicating the importance of Cav1 in normal mucosal repair after injury.


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)

Histological appearance and macroscopic damage of gastric mucosa after exposure to hypertonic NaCl in mice. Gastric mucosal injury was induced by intragastric administration of 3.4 mol/L NaCl as described in Material and Methods section. Mice were euthanized during recovery from injury at 0, 3, 6, and 16 h after the administration of NaCl. (A) Paraffin‐embedded sections with H/E staining from different times after injury. Scale bar, 100 μm. Original magnification ×100. (B) Ulcer index in gastric mucosa after injury. Values are means ± SEM from four to five mice/group. *P < 0.05 compared with control littermates.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig02: Histological appearance and macroscopic damage of gastric mucosa after exposure to hypertonic NaCl in mice. Gastric mucosal injury was induced by intragastric administration of 3.4 mol/L NaCl as described in Material and Methods section. Mice were euthanized during recovery from injury at 0, 3, 6, and 16 h after the administration of NaCl. (A) Paraffin‐embedded sections with H/E staining from different times after injury. Scale bar, 100 μm. Original magnification ×100. (B) Ulcer index in gastric mucosa after injury. Values are means ± SEM from four to five mice/group. *P < 0.05 compared with control littermates.
Mentions: Second, we examined changes in the rate of gastric mucosal repair and the levels of Cav1/TRPC1 complexes in the mucosal tissue after exposure to hypertonic NaCl as described previously (Coimbra et al. 1997; Tatemichi et al. 2003). Exposure of the gastric mucosa to 3.4 mol/L NaCl induced visible lesions in littermate and Cav1−/− mice. Histological examination (Fig. 2A) and macroscopic damage (Fig. 2B) showed that the maximal mucosal injury occurred 3 h after intragastric administration of hypertonic NaCl and that the repair process began 6 h and was almost completed 16 h in littermate mice. However, target deletion of the Cav1 gene significantly delayed gastric mucosal repair of hypertonic NaCl‐induced injury. We have also examined changes in mucosal injury at 1 and 2 h after the exposure to NaCl and found no significant damage to gastric mucosa (data not shown). At 16 h after administration of hypertonic NaCl, visible lesions in the gastric mucosa were still noticeable in Cav1−/− mice (Fig. 2Ab, right panel), indicating the importance of Cav1 in normal mucosal repair after injury.

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