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Title 

Phenotype of a calbindin-D9k gene knockout is compensated for by the induction of other calcium transporter genes in a mouse model

Authors 

G S LeeKun Yeong LeeK C ChoiY H RyuS G PaikG T OhE B Jeung

Publisher 

American Society for Bone and Mineral Research

Issue Date 

2007

Citation 

Journal of Bone and Mineral Research, vol. 22, no. 12, pp. 1968-1978

Keywords 

calbindin-D9kcalcium-binding proteinsknockout miceTRPV6adenosine triphosphatasecalbindincalcium binding proteinvanilloid receptor 5adenosine triphosphatase (calcium)Calb1 protein, mouse

Abstract 

CaBP-9k may be involved in the active calcium absorption and embryo implantation. Although we generated CaBP-9k KO mice to explore its function, no distinct phenotypes were observed in these KO mice. It can be hypothesized that TRPV5 and 6 and plasma membrane calcium ATPase 1b may play a role in the regulation of calcium transport to compensate CaBP-9k deficiency in its KO model. Introduction: Active calcium transport in the duodenum and kidney is carried in three steps: calcium entry through epithelial Ca2+ channels (TRPV5 and TRPV6), buffering and/or transport by calbindin-D9k (CaBP-9k) and -D28k (CaBP-28k). and extrusion through the plasma membrane calcium ATPase 1b (PMCA1P) and sodium/calcium exchanger 1. Although the molecular mechanism of calcium absorption has been studied using knockouts (KOs) of the vitamin D receptor and CaBP-28k in animals, the process is not fully understood. Materials and Methods: We generated CaBP-9k KO mice and assessed the phenotypic characterization and the molecular regulation of active calcium transporting genes when the mice were fed different calcium diets Results: General phenotypes showed no distinct abnormalities. Thus, the active calcium transport of CaBP-9k-null mice procceded normally in this study. Therefore, the compensatory molecular regulation of this mechanism was elucidated. Duodenal TRPV6 and CaBP-9k mRNA of wildtype (WT) mice increased gradually during preweaning. CaBP-9k is supposed to be an important factor in active calcium transport, but its role is probably compensated for by other calcium transporter genes (i.e., intestinal TRPV6 and PMCA1b) during preweaning and renal calcium transporters in adult mice. Conclusions: Depletion of the CaBP-9k gene in a KO mouse model had little phenotypic effect, suggesting that its depletion may be compensated for by calcium transporter genes in the intestine of young mice and in the kidney of adult mice.

ISSN 

0884-0431

Link 

http://dx.doi.org/10.1359/jbmr.070801

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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