CHAPTER 5 Delayed microvascular shear adaptation in Pulmonary Arterial Hypertension : role of Platelet Endothelial Cell Adhesion Molecul-1 cleavage

Altered pulmonary hemodynamics and high fluid shear stress (HSS) are characteristic hallmarks in the pathogenesis of Pulmonary Arterial Hypertension (PAH). However, the contribution of HSS to cellular and vascular alterations in PAH is unclear. We hypothesize that failing shear adaptation is an essential part of the endothelial dysfunction in all forms of PAH and tested whether microvascular (MVEC) respectively arterial endothelial cells (PAEC) from PAH patient lungs adapt to HSS and if the shear defect partakes in vascular remodeling