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The rapid nongenomic actions of 1α,25‐dihydroxyvitamin D 3 modulate the hormone‐induced increments in osteocalcin gene transcription in osteoblast‐like cells
Author(s) -
Baran Daniel T.,
Sorensen Ann Marie,
Shalhoub Victoria,
Owen Thomas,
Stein Gary,
Lian Jane
Publication year - 1992
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.240500203
Subject(s) - osteocalcin , calcitriol receptor , osteoblast , intracellular , gene expression , biology , messenger rna , transcription (linguistics) , medicine , endocrinology , hormone response element , vitamin d and neurology , microbiology and biotechnology , chemistry , gene , biochemistry , alkaline phosphatase , enzyme , in vitro , estrogen receptor , genetics , linguistics , philosophy , cancer , breast cancer
Abstract We have previously shown that one of the rapid nongenomic actions of 1α,25‐dihydroxyvitamin D 3 (1α,25‐(OH) 2 D 3 ), the increase in intracellular calcium (Ca 2+ ), accompanies the increased osteocalcin (OC) mRNA steady‐state levels in rat osteosarcoma cells. To determine the functional significance of the nongenomic actions, we have measured changes in intracellular Ca 2+ as an indicator of the rapid effects and have assessed the effect of inhibition of the rapid increase in cellular Ca 2+ by the inactive epimer, 1β,25‐dihydroxyvitamin D 3 (1β,25‐(OH) 2 D 3 ) on OC mRNA steady‐state levels and transcription. 1β,25‐dihydroxyvitamin D 3 inhibited 1α,25‐(OH) 2 D 3 induced increases in intracellular Ca 2+ and OC mRNA transcription at 1 hr and OC mRNA steady state levels at 3 hr. 1β,25‐Dihydroxyvitamin D 3 did not alter the binding of the vitamin D receptor complex to the vitamin D responsive element of the OC gene. The results demonstrate the functional importance of the rapid, nongenomic actions of 1α,25‐(OH) 2 D 3 in the genomic activation of the OC gene by the hormone in rat osteoblast‐like cells, perhaps by modifying subtle structural and/or functional properties of the vitamin D–receptor DNA complex or by affecting other protein DNA interactions that support OC gene transcription. © 1992 Wiley‐Liss, Inc.