Influence of endothelial Cx40 under atheroprone and atheroprotective flow

High laminar shear stress (HLSS), as observed in straight parts of arteries, assures a quiescent non-activated endothelium through the induction of the Krüppel-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. Mouse ECs (bEnd.3) were exposed to static conditions, high LSS (HLSS; 20 dynes/cm2), or oscillatory SS (OSS; 5 dynes/cm2, 1Hz) for 48 hours using an Ibidi flow system. Knock-down of KLF4 or Cx40 was performed using siRNA.