Project description:Caskin2 is a previously uncharacterized gene encoding a predicted scaffolding protein that we have found is highly expressed in vascular endothelial cells. We used microarray to identify genes that are differentially expressed in the setting of Caskin2 overexpression to test the hypothesis that Caskin2 expression induces a quiescent gene expression profile in cultured endothelial cells.
Project description:Advanced glycation end products (AGEs) in diabetes can cause endothelial damage. Heparin, widely known as a recognized anticoagulant, is also a multifunctional therapeutic drug. This study investigated whether heparin could ameliorate AGEs-induced endothelial injury. Remarkably, heparin effectively attenuated this cellular damage and assumed a reparative role. Furthermore, heparin inhibited the AGEs-RAGE-NFκB axis, thereby mitigating endothelial inflammatory injury. Comprehensive proteome and knockdown experiments suggested that heparin may exert a positive influence on cell growth and further alleviate pathological damage by upregulating the expression of LYAR (Cell growth-regulating nucleolar protein). Diabetic mouse model was also used to further verify the changes of endothelial tissue in diabetic state and heparin intervention. In summary, these findings demonstrate that heparin has the potential to ameliorate AGEs-induced endothelial injury, opening new avenues for exploring the expanded therapeutic roles of heparin and its potential application in the management of diabetes and its associated complications.
Project description:One of the hallmarks in hypertension is a pressure-induced change in endothelial cell phenotype. A cytoskeletal protein zyxin, which was seen to translocate from focal adhesion contacts to the nucleus in response to the increased wall tensionis, mediates the tension-induced endothelial signaling. Microarrays were used to detail the role of zyxin in the tension-induced expression changes in endothelial cells. Primary endothelial cells (Huvec) from four treatment groups were used for RNA extraction and hybridization on Affymetrix microarrays: wild type under normal condition, wild type under tension, Zyxin-SiRNA-treated under normal condition and Zyxin-SiRNA-treated under tension.
Project description:One of the hallmarks in hypertension is a pressure-induced change in endothelial cell phenotype. A cytoskeletal protein zyxin, which was seen to translocate from focal adhesion contacts to the nucleus in response to the increased wall tensionis, mediates the tension-induced endothelial signaling. Microarrays were used to detail the role of zyxin in the tension-induced expression changes in endothelial cells.