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Cell Biol Toxicol. 2009 Jun;25(3):297-308. doi: 10.1007/s10565-008-9084-8. Epub 2008 Jun 19.

Role of Yersinia enterocolitica heat-stable enterotoxin (Y-STa) on differential regulation of nuclear and cytosolic calcium signaling in rat intestinal epithelial cells.

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Division of Pathophysiology, National Institute of Cholera and Enteric Diseases, Calcutta, India.


The heat-stable enterotoxin (Y-STa) produced by the pathogenic strains of Yersinia enterocolitica is a causative agent of secretory diarrhea. We have reported earlier that Y-STa-induced inositol trisphosphate-mediated cytosolic calcium rise occurs in rat intestinal epithelial cells. In the present communication, the involvement of a nuclear calcium store in the action mechanism of Y-STa in rat intestinal epithelial cells has been shown. Calcium imaging with time series confocal microscopy shows that Y-STa stimulates both the nuclear and cytosolic calcium levels in rat intestinal epithelial cells where a rise in nuclear calcium precedes the cytosolic events. Moreover, Y-STa stimulates both cytosolic and nuclear inositol trisphosphate (IP(3)) levels in a time-dependent manner. Western blot and immunocytochemical analysis reveal a higher density of IP(3) receptor type II in the nuclear membrane compared to the cytosol, which may be the cause of an early rise of the nuclear calcium level. Therefore, it is suggested that Y-STa regulates the nuclear and cytosolic calcium signals in a distinct temporal manner in rat intestinal epithelial cells.

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