3.8 Article

Altered renin synthesis and secretion in the kidneys of heterozygous mice with a null mutation in the TGF-beta(2) gene

Journal

EXPERIMENTAL NEPHROLOGY
Volume 10, Issue 5-6, Pages 374-382

Publisher

KARGER
DOI: 10.1159/000065302

Keywords

transforming growth factor-beta(2); heterozygous deficient mice; kidneys; renin synthesis and secretion

Funding

  1. EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD026471] Funding Source: NIH RePORTER
  2. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL041496] Funding Source: NIH RePORTER
  3. NHLBI NIH HHS [HL41496] Funding Source: Medline
  4. NICHD NIH HHS [HD26471] Funding Source: Medline

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Transforming growth factors beta (TGF-betas) are peptides involved in autocrine and paracrine control of cell growth and differentiation. In the kidneys, TGF-beta(2) has been shown to localize specifically in renin-producing cells in various conditions stimulating the renin response. To test in vivo the functional role of TGF-beta(2), the renin response was investigated in mice heterozygous for a null mutation of the TGF-beta(2) gene, which had a twofold reduction in the amount of TGF-beta(2) mRNA. Although the increase in plasma renin concentration triggered by dehydration was not different from wild-type mice, renal renin mRNA and protein levels were higher in mutant mice under hydrated or dehydrated conditions. These data suggest that TGF-beta(2) exerts an inhibitory effect on renin synthesis and release from the juxtaglomerular apparatuses. Copyright (C) 2002 S. Karger AG, Basel.

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