Fig. 3

Summary of the mechanisms involved in human cerebral microvascular endothelial cells induced by mechanical stretching. Stretch stimuli are sensed by mechanoreceptors of the endothelial cell that transduce downstream protein signals. This will result in gene activation and increased protein synthesis that alters cell phenotype and function. However, different stretch intensity, magnitude and duration may activate different mechanisms. Physiological stretch is beneficial in maintaining healthy blood vessels; however, pathological stretch, as is observed in hypertension, could activate pathways leading to disease development. Thus, it is important to understand and elucidate the signaling involved with these processes as this could aid in the identification of novel therapeutic approaches aimed at treating vascular related diseases. Ca ²⁺ Calcium ion, ECM Extracellular matrix, EDHF Endothelium derived hyperpolarizing factor, EET Epoxyeicosatrienoic acid, eNOS Endothelial nitric oxide synthase, ET-1 Endothelin 1, MCP-1 Monocyte chemoattractant protein-1, NO Nitric oxide, PECAM-1 Platelet endothelial cell adhesion molecule 1, ROS Reactive oxygen species, SA channel Stretch activated channel, TK receptors Tyrosine kinase receptors, VCAM-1 Vascular cell adhesion molecule-1, VE-cadherin Vascular endothelial cadherin, wPB Weibel-Palade Bodies