Na+-Ca2+ exchanger modulates Ca2+ content in intracellular Ca2+ stores in rat osteoblasts.
- Author:
Sang Yong JUNG
1
;
Yong Joo PARK
;
Young Jun PARK
;
Seok Ho CHA
;
Myung Za LEE
;
Chang Kook SUH
Author Information
1. Department of Physiology and Biophysics, Center for Advanced Medical Education by BK21 Project, Inha University College of Medicine, Incheon 402-751, Korea. cksuh@inha.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
calcium;
osteoblasts;
sodium-calcium exchanger
- MeSH:
Alkaline Phosphatase/metabolism;
Animals;
Calcium/*metabolism;
Cell Membrane/metabolism;
Cell Survival;
Cells, Cultured;
Cytoplasm/metabolism;
Endoplasmic Reticulum/metabolism;
Intracellular Space/metabolism;
Oligodeoxyribonucleotides, Antisense/pharmacology;
Osteoblasts/drug effects/*physiology;
Rats;
Signal Transduction;
Sodium/physiology;
Sodium-Calcium Exchanger/*physiology
- From:Experimental & Molecular Medicine
2007;39(4):458-468
- CountryRepublic of Korea
- Language:English
-
Abstract:
Na+ -Ca2+ exchanger (NCX) transports Ca2+ coupled with Na+ across the plasma membrane in a bi-directional mode. Ca2+ flux via NCX mediates osteogenic processes, such as formation of extracellular matrix proteins and bone nodules. However, it is not clearly understood how the NCX regulates cellular Ca2+ movements in osteogenic processes. In this study, the role of NCX in modulating Ca2+ content of intracellular stores ([Ca2+](ER)) was investigated by measuring intracellular Ca2+ activity in isolated rat osteoblasts. Removal of extracellular Na+ elicited a transient increase of intracellular Ca2+ concentration ([Ca2+](i)). Pretreatment of antisense oligodeoxynucleotide (AS) against NCX depressed this transient Ca2+ rise and raised the basal level of [Ca2+](i). In AS-pretreated cells, the expression and activity of alkaline phosphatase (ALP), an osteogenic marker, were decreased. However, the cell viability was not affected by AS-pretreatment. Suppression of NCX activity by the AS-pretreatment decreased ATP-activated Ca2+ release from intracellular stores and significantly enhanced Ca2+ influx via store operated calcium influx (SOCI), compared to those of S-pretreated or control cells. These results strongly suggest that NCX has a regulatory role in cellular Ca2+ pathways in osteoblasts by modulating intracellular Ca2+ content.
