Angiotensin II-induced mitochondrial reactive oxygen species and peroxiredoxin-3 expression in cardiac fibroblasts

作者：Lijnen Paul J^*; Piccart Yvette; Coenen Tamara; Prihadi John S

来源：Journal of Hypertension, 2012, 30(10): 1986-1991.

DOI：10.1097/HJH.0b013e32835726c1

• angiotensin II
• cardiac fibroblasts
• mitochondria
• peroxiredoxin-3
• reactive oxygen species

Objective: The aim of this study was to determine whether angiotensin II (ANG II) affects the protein and mRNA expression of the mitochondrial antioxidant peroxiredoxin-3 (Prx-3) in cardiac fibroblasts, thereby contributing to the oxidative stress in the myocardium. %26lt;br%26gt;Method: Cardiac fibroblasts (passage 2) from normal male adult rats were cultured to confluency and incubated in Dulbecco%26apos;s modified Eagle%26apos;s medium for 24h. The cells were then preincubated with(out) the tested inhibitors for 1 h and further incubated with/without ANG II (1 mu mol/l) for 24h. %26lt;br%26gt;Results: ANG II increased (P %26lt; 0.001) the mitochondrial production of reactive oxygen species in cardiac fibroblasts from 187.8 +/- 38.6 to 313.8 +/- 30.6 a.u./mg mitochondrial protein (n = 15). ANG II decreased (P %26lt; 0.01) the mRNA and protein expression of Prx-3 by 36.9 +/- 3.0% and 29.7 +/- 2.7% (n = 4), respectively. The ANG II-induced decrease in mRNA expression of Prx-3 was prevented by the angiotensin type 1 receptor blocker, losartan but not by the angiotensin type 2 receptor blocker, PD 123319. %26lt;br%26gt;Conclusion: Our data indicate that ANG II-stimulated mitochondrial reactive oxygen species production in rat cardiac fibroblasts is accompanied by a reduction in the expression of the mitochondria! antioxidant Prx-3, and thereby potentially contributing to oxidative stress in the myocard.

• 出版日期2012-10
• 单位KU Leuven