Phosphorylation of PTEN increase in pathological right ventricular hypertrophy in rats with chronic hypoxia induced pulmonary hypertension.

Background: Phosphatase and tensin homologue on chromosome ten (PTEN) acts as a convergent nodal signalling point for cardiomyocyte hypertrophy, growth and survival. However, the role of PTEN in cardiac conditions such as right ventricular hypertrophy caused by chronic hypoxic pulmonary, hypertension remains unclear. This study preliminarily discussed the role of PTEN in the cardiac response to increased pulmonary vascular resistance using the hypoxia-induced PH rats.

Methods: Male Sprague Dawley rats were exposed to 10% oxygen for 1, 3, 7, 14 or 21 days to induce hypertension and right ventricular hypertrophy. Right ventricular systolic pressure was measured via catheterization. Hypertrophy index was calculated as the ratio of right ventricular mass to left ventricle plus septum mass. Tissue morphology and fibrosis were measured using hematoxylin, eosin and picrosirius red staining. The expression and phosphorylation levels of PTEN in ventricles were determined by real time PCR and Western blotting.

Results: Hypoxic exposure of rats resulted in pathological hypertrophy, interstitial fibrosis and remodelling of the right ventricle. The phosphorylation of PTEN increased significantly in the hypertrophic right ventricle compared to the normoxic control group. There were no changes in protein expression in either ventricle.

Conclusion: Hypoxia induced pulmonary hypertension developed pathological right ventricular hypertrophy and remodelling probably related to an increased phosphorylation of PTEN.