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Related Experiment Videos

Ovine 11 beta-hydroxysteroid dehydrogenase: from gene to function

K Yang1

  • 1Lawson Research Institute, St. Joseph's Hospital, Department of Ob/Gyn, University of Western Ontario, London, Canada.

Endocrine Research
|February 1, 1995
PubMed
Summary

Two forms of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) were found in sheep liver and kidney. Gene expression varied by tissue and developmental stage, with unique findings in fetal sheep development.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Developmental Biology

Background:

  • 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) exists in distinct isoforms with differing enzymatic activities.
  • These isoforms play crucial roles in regulating glucocorticoid action.
  • Understanding their tissue-specific expression and developmental regulation is vital.

Purpose of the Study:

  • To identify and characterize 11 beta-HSD isoforms in ovine liver and kidney.
  • To investigate the gene expression of 11 beta-HSD1 during fetal sheep development.
  • To explore the physiological roles of 11 beta-HSD in fetal development.

Main Methods:

  • Enzymatic activity assays to distinguish 11 beta-HSD isoforms.
  • cDNA cloning of ovine 11 beta-HSD1.

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  • Gene expression analysis using the cloned cDNA as a probe in fetal sheep tissues.
  • Main Results:

    • Identified two distinct 11 beta-HSD isoforms: 11 beta-HSD1 (hepatic, reversible, NADP(H)-dependent) and 11 beta-HSD2 (renal, unidirectional, NAD-dependent).
    • Ovine placenta expressed both isoforms.
    • Fetal and adult liver were primary sites of 11 beta-HSD1 expression, showing tissue-specific and developmental regulation. Notably, sheep kidney lacked 11 beta-HSD1 mRNA and activity.
    • Two non-functional 11 beta-HSD1 variants were also identified.

    Conclusions:

    • 11 beta-HSD1 gene expression is developmentally programmed and tissue-specific in sheep.
    • The unique absence of 11 beta-HSD1 in sheep kidney suggests specialized roles.
    • 11 beta-HSD in the fetal pituitary, liver, and placenta likely influences fetal development and glucocorticoid feedback mechanisms.