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Initiation Site of Ca(2+) Entry Evoked by Endoplasmic Reticulum Ca(2+) Depletion in Mouse Parotid and Pancreatic Acinar Cells
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 dep...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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Yonsei University College of Medicine
2007
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628100/ https://www.ncbi.nlm.nih.gov/pubmed/17594163 http://dx.doi.org/10.3349/ymj.2007.48.3.526 |
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author | Jo, Hae Byun, Hae Mi Lee, Syng-Ill Shin, Dong Min |
author_facet | Jo, Hae Byun, Hae Mi Lee, Syng-Ill Shin, Dong Min |
author_sort | Jo, Hae |
collection | PubMed |
description | 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 Ca(2+) entry by depletion of the ER initiates at the basal pole in polarized exocrine cells and may help to characterize the nature of SOCC. |
format | Text |
id | pubmed-2628100 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | Yonsei University College of Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-26281002009-02-02 Initiation Site of Ca(2+) Entry Evoked by Endoplasmic Reticulum Ca(2+) Depletion in Mouse Parotid and Pancreatic Acinar Cells Jo, Hae Byun, Hae Mi Lee, Syng-Ill Shin, Dong Min Yonsei Med J Original Article 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 Ca(2+) entry by depletion of the ER initiates at the basal pole in polarized exocrine cells and may help to characterize the nature of SOCC. Yonsei University College of Medicine 2007-06-30 2007-06-20 /pmc/articles/PMC2628100/ /pubmed/17594163 http://dx.doi.org/10.3349/ymj.2007.48.3.526 Text en Copyright © 2007 The Yonsei University College of Medicine http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Jo, Hae Byun, Hae Mi Lee, Syng-Ill Shin, Dong Min Initiation Site of Ca(2+) Entry Evoked by Endoplasmic Reticulum Ca(2+) Depletion in Mouse Parotid and Pancreatic Acinar Cells |
title | Initiation Site of Ca(2+) Entry Evoked by Endoplasmic Reticulum Ca(2+) Depletion in Mouse Parotid and Pancreatic Acinar Cells |
title_full | Initiation Site of Ca(2+) Entry Evoked by Endoplasmic Reticulum Ca(2+) Depletion in Mouse Parotid and Pancreatic Acinar Cells |
title_fullStr | Initiation Site of Ca(2+) Entry Evoked by Endoplasmic Reticulum Ca(2+) Depletion in Mouse Parotid and Pancreatic Acinar Cells |
title_full_unstemmed | Initiation Site of Ca(2+) Entry Evoked by Endoplasmic Reticulum Ca(2+) Depletion in Mouse Parotid and Pancreatic Acinar Cells |
title_short | Initiation Site of Ca(2+) Entry Evoked by Endoplasmic Reticulum Ca(2+) Depletion in Mouse Parotid and Pancreatic Acinar Cells |
title_sort | initiation site of ca(2+) entry evoked by endoplasmic reticulum ca(2+) depletion in mouse parotid and pancreatic acinar cells |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628100/ https://www.ncbi.nlm.nih.gov/pubmed/17594163 http://dx.doi.org/10.3349/ymj.2007.48.3.526 |
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