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The Role of Mitophagy in Development of Pulmonary Hypertension
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A2099 - The Role of Mitophagy in Development of Pulmonary Hypertension
Author Block: A. Saraji, N. Sommer, K. Schäfer, A. Sydykov, M. Hecker, W. Seeger, A. H. Ghofrani, R. T. Schermuly, N. Weissmann, O. Pak; Internal Medicine, Excellence Cluster Cardio-Pulmonary System (ECCPS), University of Giessen and Marburg Lung Center, The German Center for Lung Research (DZL), Justus- Liebig-University, Giessen, Germany.
Rationale: Pulmonary hypertension (PH) is characterized by pulmonary vascular remodeling leading to increased pulmonary vascular resistance and ultimately to the right heart failure. Mitochondrial dysfunction plays an important role in the development of PH. Mitophagy serves to remove dysfunctional mitochondria mostly via phosphatase and tensin homolog (PTEN) - induced putative kinase 1 (PINK1). We aimed to investigate the role of mitophagy in chronic hypoxia-induced PH.
Methods: PH was investigated in wild type (WT) and in global PINK1 knockout (PINK1-/-) mice exposed for 4 weeks to 10% O2 chronic hypoxia by hemodynamics, echocardiography and morphometry. Proliferation and apoptosis of the primary pulmonary artery smooth muscle cells (PASMCs) were studied after incubation at 1% O2 hypoxia for 5 days.
Results: Protein expression of PINK1 was increased in lung homogenate from mice with chronic hypoxia-induced PH as well as in PASMCs exposed for 5 days to 1% O2. Hypoxia-induced proliferation of PINK1-/- PASMCs was decreased, while their apoptosis was increased after incubation in hypoxia compared to WT PASMCs. However, the increase in right ventricular systolic pressure, degree of right ventricle (RV) hypertrophy and RV dysfunction only tendentially differed in the WT and PINK1-/- mice after chronic hypoxic exposure.
Conclusion: Our data suggests that PINK1-mediated mitophagy could play an important role in the chronic hypoxia-induced alterations of PASMCs proliferation and apoptosis.
Author Block: A. Saraji, N. Sommer, K. Schäfer, A. Sydykov, M. Hecker, W. Seeger, A. H. Ghofrani, R. T. Schermuly, N. Weissmann, O. Pak; Internal Medicine, Excellence Cluster Cardio-Pulmonary System (ECCPS), University of Giessen and Marburg Lung Center, The German Center for Lung Research (DZL), Justus- Liebig-University, Giessen, Germany.
Rationale: Pulmonary hypertension (PH) is characterized by pulmonary vascular remodeling leading to increased pulmonary vascular resistance and ultimately to the right heart failure. Mitochondrial dysfunction plays an important role in the development of PH. Mitophagy serves to remove dysfunctional mitochondria mostly via phosphatase and tensin homolog (PTEN) - induced putative kinase 1 (PINK1). We aimed to investigate the role of mitophagy in chronic hypoxia-induced PH.
Methods: PH was investigated in wild type (WT) and in global PINK1 knockout (PINK1-/-) mice exposed for 4 weeks to 10% O2 chronic hypoxia by hemodynamics, echocardiography and morphometry. Proliferation and apoptosis of the primary pulmonary artery smooth muscle cells (PASMCs) were studied after incubation at 1% O2 hypoxia for 5 days.
Results: Protein expression of PINK1 was increased in lung homogenate from mice with chronic hypoxia-induced PH as well as in PASMCs exposed for 5 days to 1% O2. Hypoxia-induced proliferation of PINK1-/- PASMCs was decreased, while their apoptosis was increased after incubation in hypoxia compared to WT PASMCs. However, the increase in right ventricular systolic pressure, degree of right ventricle (RV) hypertrophy and RV dysfunction only tendentially differed in the WT and PINK1-/- mice after chronic hypoxic exposure.
Conclusion: Our data suggests that PINK1-mediated mitophagy could play an important role in the chronic hypoxia-induced alterations of PASMCs proliferation and apoptosis.
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