Regulation of Mitochondrial Fragmentation in Microvascular Endothelial Cells Isolated from the Su5416/Hypoxia model of Pulmonary Arterial Hypertension.

Regulation of Mitochondrial Fragmentation in Microvascular Endothelial Cells Isolated from the Su5416/Hypoxia model of Pulmonary Arterial Hypertension. Am J Physiol Lung Cell Mol Physiol. 2019 Aug 28;: Authors: Suresh K, Servinsky L, Jiang H, Bigham Z, Zaldumbide J, Huetsch JC, Kliment C, Acoba MG, Kirsch BJ, Claypool SM, Le A, Damarla M, Shimoda LA Abstract Pulmonary arterial hypertension (PAH) is a morbid disease characterized by progressive right ventricle (RV) failure due to elevated pulmonary artery pressures (PAP). In PAH, histologically complex vaso-occlusive lesions in the pulmonary vasculature contribute to elevated PAP. However, the mechanisms underlying dysfunction of the microvascular endothelial cells (MVECs) that comprise a significant portion of these lesions are not well understood. We recently showed that MVECs isolated from the rat Sugen/Hypoxia (SuHx) experimental model of PAH (SuHx-MVECs) exhibit increases in: migration/proliferation, mitochondrial ROS (mtROS) production, intracellular calcium levels ([Ca2+]i) and mitochondrial fragmentation. Furthermore, quenching mtROS with the targeted antioxidant MitoQ attenuated basal [Ca2+]I, migration and proliferation; however, whether increased mtROS was associated with increased [Ca2+]i and/or changes in mitochondrial morphology was not clear. To better understand this relationship, we measured changes in mitochondrial morphology at baseline and following inhibition of m...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - Category: Cytology Authors: Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research