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      Overexpression of angiotensinogen increases tubular apoptosis in diabetes.

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          Abstract

          The intrarenal renin-angiotensin system (RAS) plays an important role in the progression of diabetic nephropathy. We have previously reported that mice overexpressing angiotensinogen in renal proximal tubular cells (RPTC) develop hypertension, albuminuria, and renal injury. Here, we investigated whether activation of the intrarenal RAS contributes to apoptosis of RPTC in diabetes. Induction of diabetes with streptozotocin in these transgenic mice led to significant increases in BP, albuminuria, RPTC apoptosis, and proapoptotic gene expression compared with diabetic nontransgenic littermates. Insulin and/or RAS blockers markedly attenuated these changes. Hydralazine prevented hypertension but not albuminuria, RPTC apoptosis, or proapoptotic gene expression. In vitro, high-glucose medium significantly increased apoptosis and caspase-3 activity in rat immortalized RPTC overexpressing angiotensinogen compared with control cells, and these changes were prevented by insulin and/or RAS blockers. In conclusion, intrarenal RAS activation and high glucose may act in concert to increase tubular apoptosis in diabetes, independent of systemic hypertension.

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          Author and article information

          Journal
          J Am Soc Nephrol
          Journal of the American Society of Nephrology : JASN
          Ovid Technologies (Wolters Kluwer Health)
          1533-3450
          1046-6673
          Feb 2008
          : 19
          : 2
          Affiliations
          [1 ] Université de Montréal Centre hospitalier de l'Université de Montréal-Hôtel-Dieu, Research Centre Pavillon Masson, 3850 Saint Urbain Street, Montreal, Quebec, Canada H2W 1T8.
          Article
          ASN.2007010074
          10.1681/ASN.2007010074
          2396745
          18057217
          67e21591-9ca6-4383-8cde-4aa08f00f4f3
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