Background and Objective; Peroxiredoxins (Prxs) are a ubiquitous family of antioxidant enzymes that control cytokine-induced peroxide levels which mediate signal transduction in mammalian cells. But, the role and expression of Prx isoforms in cardiovascular system were unknown. We analyzed the expression and dynamic change of 2-Cys Prx redox status in myocardium with pressure overload-induced cardiac hypertrophy model.
Methods; Pressure overload-induced cardiac hypertrophy was obtained by the transverse Aortic Constriction (TAC) of Sprague-Dawley rat. Dynamic expression of 2-Cys Prx (1, 2, 3 and 4) were evaluated by Redox Western blot in heart from cardiac hypertrophy by TAC(1, 3, 5 days, 1, 2 wks; n=2 on each time point) and regression by relieving constriction(1, 3, 5days, 1, 2 wks; n=2 on each time point). Heart weight and hemodynamic profile was checked on serially.
Results; Systolic blood pressure of TAC group was significantly increased after immediate constriction and persisted up to 2 wks(195.05.0 vs 110.910.2 mmHg, p<0.01). Anatomical change of LV hypertrophy in TAC group was observed at 2weeks (septal wall thickness: 1.940.38 vs 1.280.13mm, p<0.05, LV mass/body weigh: 2.690.31 vs 2.260.28mg/g, p<0.05). In hypertrophy period of TAC, oxidized form of Prx1, 2, and 3 was significantly increased from 1 day till 1 wks and then decreased till 2 wks(relatively adapted period) where as Prx4 oxidized form increased upto 2 wks. In regression period of TAC, oxidized form of Prx1/2 was increased on 1 day, 2 wks, also Prx3/4 increased on 3 day, 2 wks. In hypertrophy period of TAC, reduced form of Prx2/3 was significantly decreased from 3 day till 2 wks and in regression period of TAC, reduced form of Prx 2, 3 and 4 was increasing from 3 day till 2 wks. In reverse, Prx3 significantly increased in 1 day.
Conclusion; 2-cys Prx system may play a crucial role in the development and regression of hypertension and LVH.