Initiation Site of Ca2+ Entry Evoked by Endoplasmic Reticulum Ca2+ Depletion in Mouse Parotid and Pancreatic Acinar Cells.
10.3349/ymj.2007.48.3.526
- Author:
Hae JO
1
;
Hae Mi BYUN
;
Syng Ill LEE
;
Dong Min SHIN
Author Information
1. Yonsei University College of Dentistry, 250 Seongsanno, Seodaemon-gu, Seoul 120-752, Korea. dmshin@yumc.yonsei.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Parotid;
Ca2+ signaling;
store-operated calcium channel
- MeSH:
Animals;
Calcium/*metabolism;
Calcium Channels/drug effects/metabolism;
Cells, Cultured;
Endoplasmic Reticulum/drug effects/*metabolism;
Mice;
Mice, Inbred ICR;
Microscopy, Fluorescence;
Pancreas/cytology/drug effects/*metabolism;
Parotid Gland/cytology/drug effects/*metabolism;
Thapsigargin/pharmacology
- From:Yonsei Medical Journal
2007;48(3):526-530
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: In non-excitable cells, which include parotid and pancreatic acinar cells, Ca(2+) entry is triggered via a mechanism known as capacitative Ca(2+) entry, or store-operated Ca(2+) entry. This process is initiated by the perception of the filling state of endoplasmic reticulum (ER) and the depletion of internal Ca(2+) stores, which acts as an important factor triggering Ca(2+) entry. However, both the mechanism of store-mediated Ca(2+) entry and the molecular identity of store-operated Ca(2+) channel (SOCC) remain uncertain. MATERIALS AND METHODS: In the present study we investigated the Ca(2+) entry initiation site evoked by depletion of ER to identify the localization of SOCC in mouse parotid and pancreatic acinar cells with microfluorometeric imaging system. RESULTS: Treatment with thapsigargin (Tg), an inhibitor of sarco/endoplasmic reticulum Ca(2+)-ATPase, in an extracellular Ca(2+) free state, and subsequent exposure to a high external calcium state evoked Ca(2+) entry, while treatment with lanthanum, a non-specific blocker of plasma Ca(2+) channel, completely blocked Tg-induced Ca(2+) entry. Microfluorometric imaging showed that Tg-induced Ca(2+) entry started at a basal membrane, not a apical membrane. CONCLUSION: These results suggest that Ca2+ entry by depletion of the ER initiates at the basal pole in polarized exocrine cells and may help to characterize the nature of SOCC.
