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Calbindin‐D28K mediates 25(OH)D3/VDR‐regulated bone formation through MMP13 and DMP1
Author(s) -
Yang LiPing,
Dong YaPing,
Luo WenTing,
Zhu Tong,
Li QiWei,
Zhang LiJun,
Kong Juan,
Yuan ZhengWei,
Zhao Qun
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26722
Subject(s) - calcitriol receptor , dmp1 , endocrinology , medicine , chemistry , downregulation and upregulation , vitamin d and neurology , osteocyte , umbilical cord , calcium , microbiology and biotechnology , biology , osteoblast , anatomy , biochemistry , gene , viral matrix protein , in vitro
Calcium binding protein calbindin‐D28K (CaBP28K) mediates the relationship between vitamin D and calcium, but its mechanism remains unclear during bone formation. The present study reports that maternal CaBP28K levels were positively correlated with paired umbilical cord CaBP28K levels. In addition, CaBP28K levels were positively correlated with the body length, and head and chest circumferences of neonates, but negatively correlated with maternal 25(OH)D3 levels. CaBP28K was also downregulated in MC3T3‐E1 osteoblasts when treated with 1,25(OH)2D or VDR overexpression, but was upregulated in the femur of 1α(OH)ase (−/−) mice. Furthermore, it was found CaBP28K may influence cell differentiation and matrix formation through the regulation of DMP1 and the interaction with MMP13 in osteoblasts. This suggests that CaBP28K could be a candidate for the negative role of 1,25(OH)2D/VDR in regulating bone mass.