Expression of Pro-Fibrotic Factors in Cardiac Tissue of Wistar and Sprague–Dawley Rats during the Development of Chronic Kidney Disease

The development of uremic cardiomyopathy (UC) and cardiac fibrosis in chronic kidney disease (CKD) was comparatively analyzed in model experiments on SPF males of Sprague–Dawley and Wistar rats. CKD was induced by left subtotal nephrectomy (NE) followed after 2 weeks by right radical NE. Sham-operated (Sham) animals served as controls. Four weeks after radical NE, blood pressure (BP) was measured, and the expression of pro-fibrotic factors (Fli1, pro-collagen I, collagen I, collagen IV) in left ventricular myocardial tissue was assessed by real-time PCR and immunoblotting. After NE, Sprague–Dawley rats exhibited a significant increase in systolic BP, as well as left ventricular hypertrophy. In Wistar rats, the difference between BP in NE and Sham animals was smaller, while the left ventricular mass to body weight ratio did not change. Experimental CKD in Sprague–Dawley rats was accompanied by a 1.5–2.5-fold suppression of Fli1 gene expression and a decrease in Fli1 protein content in cardiac muscle tissue, while no significant differences were observed in Wistar rats. Pro-collagen I and collagen I levels in the heart of rats of both strains changed at neither transcription nor translation levels. Such a difference in the development of pathological processes indicates an ineffectiveness of the applied type of NE to induce UC and investigate pro-fibrotic processes in Wistar vs. Sprague–Dawley rats.