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25 PAH-induced RVF and interstitial myocardial fibrosis Pressure overload�Cinduced RVH is associated with differentiation of fibroblasts to myofibroblasts that proliferate rapidly and secrete large quantities of collagen.31 The normally prevalent collagen III, which confers elastic properties, is replaced by collagen I that is inelastic, thereby impairing diastolic relaxation.32 In rats with RVF, by ��4 weeks after monocrotaline (MCT) injection (60 mg/kg), RV fibrosis had occurred in the epicardial layers (17% �� 2% vs. 1.5% �� 0.4%; P Crenolanib datasheet P click here that in the RV of MCT-treated (80 mg/kg) hearts, at 4 weeks after MCT injection, tenascin-C (TNC) was expressed at the messenger RNA level and at the protein level (from 0.0 to 0.62 �� 0.64 ng/mg). In the heart, TNC is an extracellular matrix glycoprotein that is expressed during cardiogenesis but disappears in the myocardium after birth. TNC may reappear in the heart under various pathological conditions, including acute myocardial infarction (MI), Pembrolizumab price myocarditis, and dilated cardiomyopathy.36 In rats with MCT-induced RVF, Umar et al.37 demonstrated that the high TNC levels in RV myocardium at 4 weeks after MCT injection were almost absent if treated with MSCs at day 14. These studies demonstrate that PAH is associated with pathological RVH and interstitial RV fibrosis that both reverse upon cell therapy with stem and progenitor cells. PAH-induced RVF and arrhythmogenesis At ��4 weeks after MCT injection, cardiomyocytes isolated from hypertrophied RVs had prolonged their action potential duration (APD90) from 33 �� 6 ms (control) to 57 �� 8 ms (P