Fig. 1.
Retinoic acid-related orphan receptor-α (RORα)sg/sg mice display exaggerated pathological hypertrophy after 14-day angiotensin II (ANG II) infusion. Wild-type (WT) and RORαsg/sg mice were treated with ANG II (2 mg·kg−1·day−1) or vehicle control (VC) by osmotic minipump for 14 days. A: heart sections were stained with wheat germ agglutinin (WGA; green), isolectin B4 (red), and DAPI (blue). Cardiomyocyte cross-sectional area (CSA) was analyzed with ImageJ software (≥4 random areas in ≥3 mice/group). The ANG II-treated CSA was indexed to the vehicle-treated CSA. B: heart weight (mg) was indexed to tibia length (mm). C: heart sections were stained with Masson trichrome. The percentage of fibrosis (trichrome blue) was determined algorithmically using Aperio ImageScope (3 sections in ≥3 mice/group). D: echocardiography compared fractional shortening in WT and RORαsg/sg mice treated with VC or ANG II. E and F: quantitative RT-PCR (n = 3–4 per group; E) and immunoblot analysis (F) comparing the abundance of RORα in ANG II- and VC-treated mouse hearts. G: immunoblot analysis for RORα in primary neonatal rat ventricular myocytes (NRVMs) and rat cardiac fibroblast (rCFBs). *P < 0.05; **P < 0.01; ***P < 0.005; ****P < 0.001. Four-group comparisons used two-way ANOVA; two-group comparisons used an unpaired t-test.