Angiotensin II plays a pathogenic role in immune-mediated renal injury in mice

阅读量：

作者：

Y Hisada，T Sugaya，M Yamanouchi，H Uchida，K Murakami

展开

摘要：

Several lines of evidence show the importance of (AII) in renal injuries, especially when hemodynamic abnormalities are involved. To elucidate the role of AII in immune-mediated renal injury, we studied anti-glomerular (GBM) in AII type 1a receptor (AT1a)-deficient homozygous (AT1a-/-) and wild-type (AT1a+/+) . A transient activation of the renin-system () was observed in both groups of at around day 1. A renal expression of () was transiently induced at six hours in both groups, which was then downregulated at day 1. In the AT1a+/+ , after activation, the glomerular expression of was exacerbated at days 7 and 14. Thereafter, severe developed, and the renal expressions of transforming growth factor-beta1 () and increased, resulting in severe and . In contrast, glomerular expression of , , and tissue damage were markedly ameliorated in the AT1a-/- . Because this amelioration is likely due to the lack of AT1a, we can conclude that AII action, mediated by AT1a, plays a pathogenic role in anti-GBM , in which AII may contribute to the exacerbation of glomerular expression. These results suggest the involvement of AII in immune-mediated renal injuries.

展开

关键词：

Animals Mice, Inbred C57BL Mice, Knockout Mice Anti-Glomerular Basement Membrane Disease Collagen Transforming Growth Factor beta Renin-Angiotensin System Chemokine CCL2 Angiotensin II