Objective:To discuss the effect of knock-out MG53 on skeletal muscle,and to determine whether MG53 can protect skeletal muscle from injury during delayed onset muscle damage(DOMS).Method:Eighty-four eight-week old C57 mice were divided into two groups due to their gene (WT and KO),and each group were divided into 7 subgroups again.14 groups,6 mice in each.They were WC,WE0,WE2,WE12,WE24,WE48,WE72 and KC,KE0,KE2,KE12,KE24,KE48,KE72.At each time point after 3 days eccentric exercise,the mice were decapitated after drawing blood.The rectus femoris of left leg was used to detect the level of MG53 with Western blot,the other side were used to do electron microscope analysis.Blood CK were measured also.Result:The CK of K0 raised remarkably and decreased gradually until W 12.But the second peak appear at W24 and decreased again gradually since then.Ultrastructural changes of skeletal muscle after eccentric exercise at different time points is obvious.The injury is worsen gradually from Wo to W24,and improved gradually from W48 to W72.Comparing with W groups,the injury in K group were even worsen an each time point.The MG53 of W0 and W24 were 16％ and 11％ higher than those before exercise (p＜0.05)and restored to normal in 72 hours after exercise.Conclusion:The injury after severe exercise is more severity in MG53 knock-out mouse than those in wild mouse.and the MG53 protein increased significantly.It suggests that MG53 may significantly relieve the skeleton muscle injury in delayed muscle sore period.

Comparing the cardiovascular disease in onion-growing region with those in non-onion-growing region, we found that, the people in these two regions are similar in their living standard, economic income and dietary habits and customs. The death rates caused by cardiovascular disease in these two regions were 0.57‰ and 1.67‰ respectively. There were markedly different incidences (p

Objective To explore the effect of exercise on vascular smooth muscle cell(VSMC) phenotype switching in hypertensive arteries and to figure out the regulatory mechanisms of mircroRNA (miR)-143/145 on Akt signaling during the process.Methods Three-month old(Wistar Kyoto rats) WKY and (spontaneously hypertensive rats) SHR were divided into 4 groups:WKY-C,SHR-C,WKY-E,and SHR-E,which were subjected to 8wk moderate treadmill training (E) or sedentary as control (C) with blood pressure being monitored.After the last bout of exercise,mesenteric arteries were isolated to determine VSMC phenotypic marker,miR143/145 expression and Akt phosphorylation.In transfection experiment in vitro,miR-145 mimic and miR-145 inhibitor were transfected into cultured VSMC,and given immunofluorescent staining using α-actin to detect the cell morphology.VSMC phenotype marker,Akt phosphorylation,and mRNA expressions of the insulin-like growth factor Ⅰ receptor (IGF-IR),Insulin receptor substrate 1 antibody(IRS-1),and p70S6K were determined.Results The blood pressure of SHR-E reduced significantly compared with that of SHR-C(P＜0.05),and the arterial thicknessof SHR-E decreased significantly (P＜0.05).The VSMC contractile marker calponin in SHR-E increased significantly when compared with SHR-C(P＜0.05),while the proliferative marker osteoppontin (OPN) in SHR-E reduced significantly than that in SHR-C(P＜0.05).The miR-145 of SHR-E was significantly enhanced(P＜0.05),while there was no significant difference in the miR-143.The Akt of SHR-E was activated more significantly than SHR-C(P＜0.05).The miR-145 overexpression by transfecting miR-145 mimic into VSMC increased α-actin significantly(P＜0.05),while miR-145 inhibitor made α-actin a decrease.Akt activation was significantly inhibited by miR-145 mimic and enhanced by miR-145 inhibitor(P＜0.05).The miR-145 significantly inhibited IRS-1 and IGF-1R mRNA(P＜ 0.05),but the targeting effects were not significant on p70S6K mRNA.Conclusions Exercise ameliorates the high blood pressure and remodels arterioles,which may rely on its regulatory role on VSMC switching from proliferative to contractile phenotype,and miR-145 is involved in this process.However,the Akt activation is not caused by the overexpression of miR-145,but through other means to promote the above VSMC switching.