Inflammatory monocyte response due to altered wall shear stress in an isolated femoral artery model.

Arteriogenesis (collateral formation) is accompanied by a pro-inflammatory state that may be related to the wall shear stress (WSS) within the neo-collateral vessels. Examining the pro-inflammatory component or is complex. In an mouse femoral artery perfusion model, we examined the effect of wall shear stress on pro-arteriogenic inflammatory markers and monocyte adhesion. In a femoral artery model with defined pulsatile flow, WSS was controlled (at physiological stress, 1.4×, and 2× physiological stress) during a 24 h perfusion before gene expression levels and monocyte adhesion were assessed. Significant upregulation of expression was found for the cytokine TNFα, adhesion molecule ICAM-1, growth factor TGFβ, and the transcription factor Egr-1 at varying levels of increased WSS compared to physiological control. Further, trends toward upregulation were found for FGF-2, the cytokine MCP-1 and adhesion molecules VCAM-1 and P-selectin with increased WSS. Finally, monocytes adhesion increased in response to increased WSS. We have developed a murine femoral artery model for studying changes in WSS and show that the artery responds by upregulating inflammatory cytokines, adhesion molecules and growth factors consistent with previous findings.