Class A scavenger receptor （SR-A） plays an important role in macrophage adhesion. However, the underlying mechanism remains unclear. We previously found that 78 kDa glucose-regulated protein （GRP78） inhibited SR- A-mediated ligand internalization into macrophage by binding to SR-A. The aim of the study was to investigate whether GRP78 could regulate SR-A-mediated cell adhesion. We demonstrated that GRP78 bound directly to SR-A by fluorescence resonance energy transfer （FRET） assay. Overexpression of GRP78 inhibited macrophage adhesion via SR-A. These results suggest that GRP78 may act as an inhibitor of macrophage adhesion via SR-A.
Macrophage death in advanced atherosclerosis promotes plaque necrosis and destabilization.Involvement of autophagy in bulk degradation of cellular components has been recognized recently as an important mechanism for cell survival under endoplasmic reticulum（ER） stress.We previously found that the engagement of class A scavenger receptor（SR-A） triggered JNK-dependent apoptosis in ER-stressed macrophages.However,pro-apoptotic mechanisms mediated by SR-A are not fully understood.Therefore,we sought to see if SR-A mediated apoptosis was associated with autophagy in macrophages.Here,we showed that fucoidan inhibited microtubule-associated protein light chain 3-phospholipid conjugates（LC3-Ⅱ） formation as well as the number of autophagosomes under ER stress.The inhibition of LC3-Ⅱ formation was paralleled by the activation of the mTOR pathway,and the inhibition of mTOR allowed LC3-Ⅱ induction in macrophages treated with thapsigargin plus fucoidan.Furthermore,apoptosis induced by fucoidan was prevented under ER stress by the mTOR inhibitor.We propose that fucoidan,a SR-A agonist,may contribute to macrophage apoptosis during ER stress by inhibiting autophagy.
Glycine is a well-documented cytoprotective agent.However,whether it has a protective effect against myocar-dial ischemia-reperfusion injury in vivo is still unknown.By using an open-chest anesthetized rat model,we found that glycine reduced the infarct size by 21% in ischemia-reperfusion injury rats compared with that in the vehicle-treated MI/R rats.The left ventricular ejection fraction and fractional shortening were increased by 19.11% and 30.98%,respectively,in glycine-treated rats.The plasma creatine kinase levels in ischemia-reperfusion injury rats decreased following glycine treatment.Importantly,administration of glycine significantly inhibited apoptosis in post-ischemia-reperfusion myocardium,which was accompanied by suppression of phosphorylated p38 mitogen-activated protein kinase and c-Jun NH2-terminal kinase,as well as the Fas ligand.These results suggest that gly-cine attenuates myocardial ischemia-reperfusion injury in vivo by inhibiting cardiomyocytes apoptosis.
