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Regulation of calbindin‐D 28K gene expression in the chick intestine: Effects of serum calcium status and 1,25‐dihydroxyvitamin D 3
Author(s) -
Hall Alan K.,
Norman Anthony W.
Publication year - 1990
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650050405
Subject(s) - calbindin , calcium , endocrinology , medicine , vitamin d dependent calcium binding protein , vitamin d and neurology , calcium binding protein , calcitriol , calcitonin , trpv6 , vitamin , dot blot , biology , calcium metabolism , chemistry , biochemistry , gene
Abstract Calbindin‐D 28K is a member of a superfamily of calcium binding proteins that share a common avidity for the divalent calcium ion. The ambient concentration of calcium in the blood circulation is thought to orchestrate the release of parathyroid hormone and calcitonin and to govern the activity of renal 1‐hydroxylase and thereby synthesis of 1,25‐dihydroxyvitamin D 3 . We report here the results of experiments designed to assess the possible contribution of dietary calcium status upon calbindin‐D 28K gene expression in the intestine of vitamin D‐deficient chicks. The actions of 1,25‐dihydroxy vitamin D 3 [1,25‐(OH) 2 D 3 ] and dietary calcium intake upon intestinal calbindin‐D 28K and calbindin‐D 28K mRNA were monitored by ELISA and dot‐blot hybridization analyses, respectively. Vitamin D 3 ‐deficient chicks were fed either a calcium‐supplemented diet (3% w/w) or a diet containing low calcium (0.4% w/w). These dietary manipulations evoked a highly significant change in serum calcium status. However, the levels of calbindin‐D 28K protein and its corresponding mRNA were unaffected. Administration of 1,25‐(OH) 2 D 3 (1‐16 nmol per animal) to both “normocalcemic” and hypocalcemic vitamin D‐deficient chicks resulted in an equivalent stimulation of duodenal calbindin‐D 28K accumulation of calbindin‐D 28K mRNA. Intestinal calbindin‐D 28K was stimulated 20‐ to 28‐fold (above control levels) by 6‐8 nmol 1,25‐(OH) 2 D 3 in both dietary treatment groups when measured 48 h after the single injection. Hence, despite the existence of a relatively large difference in serum calcium levels, the molecular actions of 1,25‐(OH) 2 D 3 in the vitamin D‐deficient animal are apparently well insulated from serum calcium chemistry. These observations support the notion that, in the absence of vitamin D 3 , the calcium ion per se is unable to modulate the calbindin‐D 28K gene in vivo.