c ‐Src kinase contributes on endothelial cells mechanotransduction in a heat shock protein 70‐dependent turnover manner

1. c ‐Src triggers proliferative and survival signals in response to a circuit of differential tensional forces; 2. Extracellular matrix remodeling‐related scenario is rigorously modulated: possible role of c‐Src on delivering signals; 3. Heat shock proteins (HSPs) were identified in response to hy pertensive stress in vitro; 4. 20S proteasome‐related genes were overexpressed and suggested protein turnover. AbstractShear stress changes are associated with a repertory of signaling cascade modulating vascular phenotype. As shear stress ‐related tensional forces might be associated with pathophysiological susceptibility, a more comprehensive molecular map needs to be addressed. Thus, we subjected human umbilical vein endothelial cells (HUVECs) to a circuit of different tensional forces in vitro considering the following three gro ups: (a) physiological blood flow shear stress condition (named Normo), (b) a hypertensive blood flow shear stress (named Hyper), and (c) these hyper‐stressed cells were returned to Normo condition (named Return). The samples were properly collected to allow different methodologies analysis. Our d ata showed a pivotal involvement of c‐Src on driving the mechanotransduction cascade by modulating signaling related with adhesion, survival (PI3K/Akt) and proliferative phenotype. Moreover, c‐Src seems to develop important role during extracellular matrix remodeling. Additionally, proteomic ana lysis showed strong involvement of heat shock pro...
Source: Journal of Cellular Physiology - Category: Cytology Authors: Tags: ORIGINAL RESEARCH ARTICLE Source Type: research