scholarly journals TRPC1‐mediated Ca 2+ signaling enhances intestinal epithelial restitution by increasing α4 association with PP2Ac after wounding

2021 ◽  
Vol 9 (9) ◽  
Author(s):  
Navneeta Rathor ◽  
Hee Kyoung Chung ◽  
Jia‐Le Song ◽  
Shelley R. Wang ◽  
Jian‐Ying Wang ◽  
...  
Keyword(s):  
Intestinal Epithelial ◽  
Epithelial Restitution

scholarly journals RhoA enhances store-operated Ca2+ entry and intestinal epithelial restitution by interacting with TRPC1 after wounding

2015 ◽  
Vol 309 (9) ◽  
pp. G759-G767 ◽  
Author(s):  
Hee Kyoung Chung ◽  
Navneeta Rathor ◽  
Shelley R. Wang ◽  
Jian-Ying Wang ◽  
Jaladanki N. Rao
Keyword(s):  
Cell Migration ◽  
Transient Receptor Potential ◽  
Ectopic Expression ◽  
Receptor Potential ◽  
Dominant Negative ◽  
Intestinal Epithelial ◽  
Epithelial Restitution ◽  
Epithelial Cell Migration ◽  
Transient Receptor ◽  
Wounded Area

Early mucosal restitution occurs as a consequence of epithelial cell migration to resealing of superficial wounds after injury. Our previous studies show that canonical transient receptor potential-1 (TRPC1) functions as a store-operated Ca2+ channel (SOC) in intestinal epithelial cells (IECs) and plays an important role in early epithelial restitution by increasing Ca2+ influx. Here we further reported that RhoA, a small GTP-binding protein, interacts with and regulates TRPC1, thus enhancing SOC-mediated Ca2+ entry (SOCE) and epithelial restitution after wounding. RhoA physically associated with TRPC1 and formed the RhoA/TRPC1 complexes, and this interaction increased in stable TRPC1-transfected IEC-6 cells (IEC-TRPC1). Inactivation of RhoA by treating IEC-TRPC1 cells with exoenzyme C3 transferase (C3) or ectopic expression of dominant negative RhoA (DNMRhoA) reduced RhoA/TRPC1 complexes and inhibited Ca2+ influx after store depletion, which was paralleled by an inhibition of cell migration over the wounded area. In contrast, ectopic expression of wild-type (WT)-RhoA increased the levels of RhoA/TRPC1 complexes, induced Ca2+ influx through activation of SOCE, and promoted cell migration after wounding. TRPC1 silencing by transfecting stable WT RhoA-transfected cells with siRNA targeting TRPC1 (siTRPC1) reduced SOCE and repressed epithelial restitution. Moreover, ectopic overexpression of WT-RhoA in polyamine-deficient cells rescued the inhibition of Ca2+ influx and cell migration induced by polyamine depletion. These findings indicate that RhoA interacts with and activates TRPC1 and thus stimulates rapid epithelial restitution after injury by inducing Ca2+ signaling.

scholarly journals Oncostatin M Mediates STAT3-Dependent Intestinal Epithelial Restitution via Increased Cell Proliferation, Decreased Apoptosis and Upregulation of SERPIN Family Members

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e93498 ◽  
Author(s):  
Florian Beigel ◽  
Matthias Friedrich ◽  
Corina Probst ◽  
Karl Sotlar ◽  
Burkhard Göke ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Family Members ◽  
Oncostatin M ◽  
Intestinal Epithelial ◽  
Epithelial Restitution

scholarly journals STIM2 Inhibits Intestinal Epithelial Restitution by Repressing STIM1‐Activated Ca 2+ Influx after Wounding

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Rao N. Jaladanki ◽  
Navneeta Rathor ◽  
Tongtong Zou ◽  
Lan Liu ◽  
Lan Xiao ◽  
...  
Keyword(s):  
Intestinal Epithelial ◽  
Epithelial Restitution

scholarly journals Polyamines regulate intestinal epithelial restitution through TRPC1-mediated Ca2+ signaling by differentially modulating STIM1 and STIM2

2012 ◽  
Vol 303 (3) ◽  
pp. C308-C317 ◽  
Author(s):  
Jaladanki N. Rao ◽  
Navneeta Rathor ◽  
Ran Zhuang ◽  
Tongtong Zou ◽  
Lan Liu ◽  
...  
Keyword(s):  
Cell Migration ◽  
Intestinal Epithelial Cell ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Intestinal Epithelial ◽  
Canonical Transient Receptor Potential ◽  
Pathological Conditions ◽  
Epithelial Restitution ◽  
Transient Receptor ◽  
Stimulation Of

Early epithelial restitution occurs as a consequence of intestinal epithelial cell (IEC) migration after wounding, and its defective regulation is implicated in various critical pathological conditions. Polyamines stimulate intestinal epithelial restitution, but their exact mechanism remains unclear. Canonical transient receptor potential-1 (TRPC1)-mediated Ca2+ signaling is crucial for stimulation of IEC migration after wounding, and induced translocation of stromal interaction molecule 1 (STIM1) to the plasma membrane activates TRPC1-mediated Ca2+ influx and thus enhanced restitution. Here, we show that polyamines regulate intestinal epithelial restitution through TRPC1-mediated Ca2+ signaling by altering the ratio of STIM1 to STIM2. Increasing cellular polyamines by ectopic overexpression of the ornithine decarboxylase (ODC) gene stimulated STIM1 but inhibited STIM2 expression, whereas depletion of cellular polyamines by inhibiting ODC activity decreased STIM1 but increased STIM2 levels. Induced STIM1/TRPC1 association by increasing polyamines enhanced Ca2+ influx and stimulated epithelial restitution, while decreased formation of the STIM1/TRPC1 complex by polyamine depletion decreased Ca2+ influx and repressed cell migration. Induced STIM1/STIM2 heteromers by polyamine depletion or STIM2 overexpression suppressed STIM1 membrane translocation and inhibited Ca2+ influx and epithelial restitution. These results indicate that polyamines differentially modulate cellular STIM1 and STIM2 levels in IECs, in turn controlling TRPC1-mediated Ca2+ signaling and influencing cell migration after wounding.

Role of Estrogen Receptor in the Regulation of Intestinal Epithelial Restitution After Mucosal Injury

2011 ◽  
Vol 140 (5) ◽  
pp. S-87
Author(s):  
Chang-Whan Kim ◽  
Tiffany A. Ornelas ◽  
Jimmy Y. Chow ◽  
Biguang Tuo ◽  
Hui Dong
Keyword(s):  
Estrogen Receptor ◽  
Mucosal Injury ◽  
Intestinal Epithelial ◽  
Epithelial Restitution

680 PP2A-Associated Protein α4 Activates Rac1 and Enhances Intestinal Epithelial Restitution by Interacting With RACK1 After Wounding

2016 ◽  
Vol 150 (4) ◽  
pp. S141
Author(s):  
Navneeta Rathor ◽  
Hee Kyoung Chung ◽  
Shelley R. Wang ◽  
Lan Liu ◽  
Lan Xiao ◽  
...  
Keyword(s):  
Intestinal Epithelial ◽  
Epithelial Restitution

Zinc (ZnSO4) stimulates intestinal epithelial restitution In vitro

1998 ◽  
Vol 114 ◽  
pp. A1132
Author(s):  
E. Cario ◽  
A. Becker ◽  
H. Goebell ◽  
A.U. Dignass
Keyword(s):  
Intestinal Epithelial ◽  
Epithelial Restitution
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