TGF-β2 appears to exert an inhibitory effect on renin synthesis and release from the juxtaglomerular apparatuses in vivo.
Answers are grounded in this paper and cite their sources.
TGF-β2 may inhibit juxtaglomerular renin in vivo; leaves open any role in human hypertension or kidney disease.
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.
No takes yet. Share an insight, caveat, or question.
Piétri et al. (2002) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: