Calcineurin A-β is required for hypertrophy but not matrix expansion in the diabetic kidney.
Bottom Line: The absence of β produced a significant decrease in total calcineurin activity in the inner medulla (IM) and reduced nuclear factor of activated T-cells (NFATc) activity.In conclusion, loss of the β isoform of calcineurin is sufficient to reproduce beneficial aspects of cyclosporine on diabetic renal hypertrophy but not matrix expansion.Therefore, while multiple signals appear to regulate matrix, calcineurin β appears to be a central mechanism involved in organ hypertrophy.
Affiliation: Department of Medicine/Division of Nephrology, Emory University School of Medicine, Atlanta, GA 30322, USA.Show MeSH
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Mentions: Next, glomerular hypertrophy was examined. As expected, the size of glomeruli significantly increased in wild-type mice after 6 weeks of diabetes (there was no change in glomerular hypertrophy after 1 week [data not shown]). Similar to results from analysis of whole kidney hypertrophy, glomerular hypertrophy was attenuated in β−/− diabetic mice (Fig. 6A and B).
Affiliation: Department of Medicine/Division of Nephrology, Emory University School of Medicine, Atlanta, GA 30322, USA.