Does macrophage-expressed group IIA secretory phospholipase A2 increase atherosclerotic lesion formation in LDL receptor-deficient mice?
Group IIA sPLA(2) can contribute to atherosclerotic lesion development through a mechanism that is independent of systemic lipoprotein metabolism.
Vein graft arterialization induces bimodal activation of extracellular-signal regulated kinase and p38(MAPK); however, in contrast with what is described in arterial injury, it does not induce c-jun N-terminal kinase activation. These results provide the first comprehensive characterization of the mitogen-activated protein kinase signaling pathways activated in vein graft arterialization and identify mitogen-activated protein kinases as potential mediators of vein graft remodeling and subsequent intimal hyperplasia.