1. Pulmonary vascular cell mitochondrial dysfunction in response to hepcidin
- Author
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Theo Issitt, S. John Wort, Gregory J. Quinlan, Quezia Toe, Miziah Mohd Ghazaly, and British Heart Foundation
- Subjects
Morphology ,medicine.medical_specialty ,Respiratory System ,Mitochondrion ,Vascular remodelling in the embryo ,Pulmonary hypertension ,Hepcidin ,medicine.artery ,Internal medicine ,Medicine ,Respiratory system ,11 Medical and Health Sciences ,chemistry.chemical_classification ,Reactive oxygen species ,Science & Technology ,biology ,business.industry ,medicine.disease ,Endocrinology ,medicine.anatomical_structure ,chemistry ,Pulmonary artery ,biology.protein ,Vascular resistance ,business ,Life Sciences & Biomedicine - Abstract
Vascular physiology predominates with endothelial cell-mediated smooth muscle responses to physiological conditions. Variations in cell-type responses are therefore important in vascular pathophysiology. Pulmonary Artery Hypertension (PAH) is characterised by vascular remodelling and proliferation of pulmonary artery smooth muscle cells (PASMC), increasing vascular resistance. Dysregulation of iron and elevated hepcidin are implicated in PAH and previously we have demonstrated hepcidin-mediated proliferation in PASMC. We hypothesise that responses to hepcidin induced iron overload are cell-type specific and we aim to comparatively analyse mitochondrial response in pulmonary arterial endothelial cells (PAEC) vs PASMC. Human PAEC or PASMC were treated with hepcidin (1 µg/ml) or IL-6 (10 ng/ml) for 24 hours. Mitochondria and mitochondrial Reactive Oxygen Species (mROS) were analysed with Mitotracker CMTMros and MitoSOX respectively, using confocal microscopy. Hepcidin treatment induced a significant reduction in fluorescence (***p =
- Published
- 2019