Initiation Site of Ca2+ Entry Evoked by Endoplasmic Reticulum Ca2+ Depletion in Mouse Parotid and Pancreatic Acinar Cells
Yonsei Medical Journal
; : 526-530, 2007.
Article
in En
| WPRIM
| ID: wpr-71485
Responsible library:
WPRO
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.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Pancreas
/
Parotid Gland
/
Calcium Channels
/
Cells, Cultured
/
Calcium
/
Thapsigargin
/
Endoplasmic Reticulum
/
Mice, Inbred ICR
/
Microscopy, Fluorescence
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Journal:
Yonsei Medical Journal
Year:
2007
Type:
Article