PLX244087

GSE118717: Influence of endothelial Cx40 under atheroprone and atheroprotective flow

• Organsim mouse
• Type RNASEQ
• Target gene
• Project ARCHS4

High laminar shear stress (HLSS), as observed in straight parts of arteries, assures a quiescent non-activated endothelium through the induction of the Krppel-like transcription factors KLF2 and KLF4. Cx40-mediated gap junctional communication contributes to a healthy endothelium by propagating adenosine-evoked anti-inflammatory signals between endothelial cells. As the promoter of the Cx40 gene contains KLF consensus binding sites, we hypothesize that HLSS through the modulation of KLF4, may affect Cx40 expression in ECs, which may affect the quiescent non-activated state of the endothelium. SOURCE: Sylvain LEMEILLEREITH University of Geneva Medical School