Loss of talin in cardiac fibroblasts results in augmented ventricular cardiomyocyte hypertrophy in response to pressure overload. Loss of talin in cardiac fibroblasts results in augmented ventricular cardiomyocyte hypertrophy in response to pressure overload

To look at the affect of talins in cardiac fibroblasts (CF), we subjected Tln2-null and Tln2-null; Tln1-specific CF knockout mice to AngII stimulation for 8 weeks to induce pressure overload injury. We found that Tln2-null; Tln1-specific CF knockout mice had increaed cardiomyocyte hypertrophy and systolic blood pressure, with not change in intersitial fibrosis. Overall design: Left Ventricle tissue was collected from Tln2-null and Tln2-null; Tln1-specific CF knockout hearts of mice treated with AngII for 8 weeks. Eeach group consisted of 8 mice (4 males and 4 females).