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Related Experiment Videos

Molecular aspects of the calbindins.

S Christakos1, R Gill, S Lee

  • 1Department of Biochemistry and Molecular Biology, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark 07103-2714.

The Journal of Nutrition
|March 1, 1992
PubMed
Summary

This study investigates how vitamin D (1,25-dihydroxycholecalciferol) and glucocorticoids regulate calbindin gene expression. Findings reveal tissue-specific responses and identify gene elements controlling calbindin regulation.

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Area of Science:

  • Molecular endocrinology
  • Gene regulation
  • Calcium homeostasis

Background:

  • Calbindin, a vitamin D-dependent calcium-binding protein, plays a crucial role in calcium absorption and transport.
  • Understanding the regulation of calbindin gene expression is essential for comprehending calcium homeostasis and potential therapeutic interventions.

Purpose of the Study:

  • To elucidate the regulatory mechanisms of calbindin gene expression by 1,25-dihydroxycholecalciferol (1,25(OH)2D3) and glucocorticoids.
  • To investigate the role of vitamin D receptor (VDR) regulation in mediating 1,25(OH)2D3's effects.
  • To identify specific DNA sequences within the calbindin gene promoter that control its expression.

Main Methods:

  • Quantitative analysis of calbindin and VDR mRNA levels in response to 1,25(OH)2D3 and dexamethasone treatment in rats.

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  • Transfection of Ros 17/2.8 cells with a mouse calbindin promoter-reporter gene construct.
  • Deletion analysis of the calbindin promoter to identify regulatory elements.

    • Main Results:

    • 1,25(OH)2D3 induces calbindin mRNA in intestine and kidney, with VDR mRNA induction observed only in vitamin D-replete animals, suggesting an inhibitor in deficient states.
    • Glucocorticoid treatment (dexamethasone) significantly decreases intestinal calbindin-D9k mRNA but does not affect kidney calbindin-D28k mRNA, indicating tissue-specific regulation.
    • Isolation of the mouse calbindin-D28k gene and identification of promoter sequences responsible for basal and hormone-inducible activity.

    Conclusions:

    • Calbindin gene expression is differentially regulated by 1,25(OH)2D3 and glucocorticoids, with distinct tissue-specific responses.
    • Vitamin D receptor regulation is influenced by the animal's vitamin D status, implying the existence of regulatory feedback mechanisms.
    • The identified promoter elements provide a foundation for further studies into the precise molecular mechanisms controlling calbindin gene expression.