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11beta-hydroxysteroid dehydrogenase activity in human aortic smooth muscle cells
H Hatakeyama1, S Inaba, I Miyamori
1Third Department of Internal Medicine, Fukui Medical University, Japan.
Summary
11beta-Hydroxysteroid dehydrogenase type 2 (11beta-HSD2) is the primary enzyme in human vascular smooth muscle cells responsible for converting cortisol to cortisone. Impaired 11beta-HSD2 activity may contribute to hypertension development.
Area of Science:
- Endocrinology
- Cardiovascular Physiology
- Molecular Biology
Background:
- 11beta-Hydroxysteroid dehydrogenases (11beta-HSD) regulate glucocorticoid activity.
- Two isoforms exist: 11beta-HSD1 (bidirectional) and 11beta-HSD2 (dehydrogenase only).
- Diminished 11beta-HSD dehydrogenase activity is observed in hypertensive rat vasculature, but the specific isoform is unknown.
Purpose of the Study:
- To determine the role of 11beta-HSD isoforms in human vascular smooth muscle cells.
- To investigate the contribution of vascular 11beta-HSD activity to hypertension pathogenesis.
Main Methods:
- Cultured human vascular smooth muscle cells.
- Manipulation of 11beta-HSD isoform expression using antisense oligonucleotides.
- Assay of 11beta-HSD dehydrogenase activity.
Main Results:
- 11beta-Hydroxysteroid dehydrogenase type 2 (11beta-HSD2) was identified as the dominant isoform.
- 11beta-HSD2 primarily functions in the dehydrogenase mode (cortisol to cortisone) in these cells.
- The study demonstrated significant 11beta-HSD2 activity in human vasculature.
Conclusions:
- 11beta-HSD2 plays a crucial role in regulating local cortisol levels within the vascular wall.
- Impairment of 11beta-HSD2 activity in vascular smooth muscle cells may be a contributing factor to the development of hypertension.
- Targeting 11beta-HSD2 could offer a novel therapeutic strategy for hypertension.