Figure 11
From: Kallikrein-related peptidase 8 is expressed in myocardium and induces cardiac hypertrophy
Administration of PAR1 or PAR2 antagonist significantly attenuated the hypertrophic effects of intra-cardiac Ad-KLK8 gene delivery in vivo.
Adenovirus particles containing KLK8 or control vector were administered to rats by intra-cardiac injection into the anterior wall of left ventricular. Rats injected by Ad-KLK8 were then treated by selective PAR1 antagonist RWJ56110 (1 mg/kg/day, i.p.) or PAR2 antagonist FSLLRY-NH2 (1 mg/kg/day, i.p.). Two weeks after intra-cardiac injection of Ad-KLK8 and Ad-control, experimental animals were used for measurements of cardiac hypertrophic markers (A–C) and cross-sectional area (D,E). (A–C) mRNA level of cardiac hypertrophic markers ANP (A), BNP (B) and Myh7(C) in the anterior wall of LV was determined by quantitative real-time RT-PCR. (D) WGA staining was performed on transverse sections of the anterior wall of LV. (E) Mean cardiomyocyte cross-sectional area was quantified using the Image-J cell area measurement software. Six rats were analyzed for each group and 30 to 40 cardiomyocytes were measured per rat (n = 200 cells/group). Scale bar: 50 μm. *P < 0.05, **P < 0.01 vs Ad-vector; #P < 0.05, ##P < 0.01 vs Ad-KLK8.
