Catalase prevents maternal diabetes-induced perinatal programming via the Nrf2-HO-1 defense system

Shiao Ying Chang, Yun Wen Chen, Xin Ping Zhao, Isabelle Chenier, Stella Tran, Alexandre Sauvé, Julie R. Ingelfinger, Shao Ling Zhang

研究成果: Article同行評審

27 引文 斯高帕斯(Scopus)

摘要

We investigated whether overexpression of catalase (CAT) in renal proximal tubular cells (RPTCs) could prevent the programming of hypertension and kidney disease in the offspring of dams with maternal diabetes. Male offspring of nondiabetic and diabetic dams from two transgenic (Tg) lines (Hoxb7-green fluorescent protein [GFP]-Tg [controls] and Hoxb7/CAT-GFP-Tg, which overexpress CAT in RPTCs) were studied from the prenatal period into adulthood. Nephrogenesis, systolic blood pressure, renal hyperfiltration, kidney injury, and reactive oxygen species (ROS) generation were assessed. Gene expression of transforming growth factorβ1 (TGFβ1), nuclear factor erythroid 2p45-related factor-2 (Nrf2), and heme oxygenase-1 (HO-1) was tested in both in vitro and in vivo studies. Renal dysmorphogenesis was observed in offspring of Hoxb7-GFP-Tg dams with severe maternal diabetes; the affected male offspring displayed higher renal ROS generation and developed hypertension and renal hyperfiltration as well as renal injury with heightened TGFβ1 expression in adulthood. These changes were ameliorated in male offspring of diabetic Hoxb7/ CAT-GFP-Tg dams via the Nrf2-HO-1 defense system. CAT promoted Nrf2 nuclear translocation and HO-1 gene expression, seen in both in vitro and in vivo studies. In conclusion, CAT overexpression in the RPTCs ameliorated maternal diabetes-induced perinatal programming, mediated, at least in part, by triggering the Nrf2-HO-1 defense system.

原文English
頁(從 - 到)2565-2574
頁數10
期刊Diabetes
61
發行號10
DOIs
出版狀態Published - 2012 十月

All Science Journal Classification (ASJC) codes

  • 內科學
  • 內分泌學、糖尿病和代謝

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