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
em En
| WPRIM
| ID: wpr-71485
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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 ANDMETHODS:
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.Palavras-chave
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Índice:
WPRIM
Assunto principal:
Pâncreas
/
Glândula Parótida
/
Canais de Cálcio
/
Células Cultivadas
/
Cálcio
/
Tapsigargina
/
Retículo Endoplasmático
/
Camundongos Endogâmicos ICR
/
Microscopia de Fluorescência
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Yonsei Medical Journal
Ano de publicação:
2007
Tipo de documento:
Article