Objective To study the effect of human G-coupled protein kinase 4(GRK4) A142V overexpression on angiotensin Ⅱ1 type(AT1 ) receptor and its-mediated proliferation of rat vascular smooth muscle cells .Methods We constructed a lentiviral vec-tor carrying human GRK4-EGFP gene and observed its expression in A10 cells .Expression of AT1 receptor were determined by im-munoblotting ,GRK4 activity were checked by spectrophotometry ;the linkage between GRK4 and AT1 receptor were determined by co-immunoprecipitation .[3 H] thymidine incorporation was used to detect changes of cell proliferation .Results As compared with the control cells ,A142V-transfected cells had higher GRK4 activity and higher AT1 receptor expression ;there was linkage between GRK4 and AT1 receptor ,the co-immunoprecipitation levels were lower in A142V cells .The basal levels of VSMC proliferation was higher in A142V cells ,Ang Ⅱ increased VSMC proliferation to a greater extent in A 142V cells .Conclusion GRK4 A142V ,via in-creasing GRK4 activity ,increases AT1 receptor expression and function in vascular smooth muscle cell proliferation .

AIM: To explore the effect of endoplasmic reticulum stress on cardiac myocyte apoptosis in mouse congestive heart failure induced by myocardial infraction.METHODS: The mouse model of heart failure was established by ligating the left anterior descending coronary to produce acute myocardial infarction.Thirty-two mice were divided into 4 groups: sham group and groups of post-operation at time points of 2,4 or 6 weeks,respectively.The ventricular dilatation and left ventricular functions were assessed by echocardiography.The expression of GRP78,CHOP,caspase-12,cleaved caspase-12,JNK and phosphorylated-JNK was detected by Western blotting.The cardiac myocyte apoptosis was determined by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling(TUNEL).RESULTS: The cardiac expression of endoplasmic reticulum chaperones GRP78 was significantly increased in the hearts with functional failure.The upregulated expression of CHOP,phosphorylated-JNK and cleaved caspase-12 illuminated that the CHOP-JNK-caspase-12 dependent pathways for endoplasmic reticulum-initiated apoptosis were activated in the heart with functional failure by myocardial infraction.CONCLUSION: These findings suggest that the congestive heart failure induced by myocardial infraction is associated with endoplasmic reticulum stress and activation of CHOP,JNK,caspase-12 dependent pathways for endoplasmic reticulum-initiated apoptosis.