Really impairs entry of extracellular calcium after a mechanical stimulus or after addition of extra calcium on the medium. How does PKD2 open in response to mechanical stress? In mammalian cells, a number of proteins associated to PKD2 have been proposed to play a key role in its activation. In ciliated cells from the kidney and vascular endothelium, the PKD1/PKD2 complex has been implicated in mechanosensing. Other results have suggested that this complex does not act as a calcium channel, but rather regulates the function of other potential channels, potentially via interactions with cytoskeleton components such as filamin. Remarkably, in Dictyostelium, PKD1 as well as TRP channels from the C and V families are absent, suggesting that PKD2 can act as a mechanosensor in the absence of other associated membrane proteins, or making use of an entirely different set of interacting partners. PKD2 may even act as a bona fide stretch-activated channel of Dictyostelium, ensuring both detection of the mechanical stress and calcium entry following activation. If new candidates implicated in mechanosensing are identified in various systems, the validity and the generality of these observations may be checked in Dictyostelium by generating the corresponding knockout strains and analyzing their phenotype. Pulmonary arterial hypertension is a vascular disease characterized by persistent precapillary pulmonary hypertension, leading to progressive right heart failure and premature death. Pulmonary hypertension can either be idiopathic or be the result of other conditions such as connective tissue disease, congenital heart disease, anorexigen use, portal hypertension, and human immunodeficiency virus. However, the pathological mechanisms underlying this condition remain elusive. Pulmonary artery endothelial cell dysfunction and structural remodeling of the pulmonary vessels are early features of PAH, characterized by a hyperproliferative and anti-apoptotic diathesis within the vascular wall of the resistant pulmonary arteries, leading to vascular lumen occlusion, right ventricular failure, and death. It has been reported that the PAH vascular remodeling process includes proliferation and migration of pulmonary artery SMCs, leading to medial hypertrophy and increased pulmonary vascular resistance. The local Y-27632 imbalance in vasoactive mediators as well as shear stress promotes proliferation and hypertrophy of endothelial and smooth muscle cells within pulmonary arterioles. Early stages of vascular remodeling include medial hypertrophy and hyperplasia, whereas the arterioles of patients with advanced PAH are characterized by complex plexiform lesions resulting from intimal hyperplasia. The terminal stage of PAH is characterized by a significant reduction in the cross sectional area of the pulmonary vasculature leading to right ventricular failure – a major factor for morbidity and mortality.