Mechanisms Of Resistin Induced Rat H9C2 Cardiomyocyte Hypertrophy Through JAK2/STAT3 Signaling Pathway

BackgroundMyocardial hypertrophy is a kind of adaptive response to pressure overload,neurohumor factor action.Early myocardial hypertrophy has some compensatory significance,but the sustained hypertrophy of cardiac muscle will lead to heart failure.Resistin is a secreted protein found in plasma and is rich in cysteine.Early studies have found that resistin can lead to disorders of glucose metabolism and is associated with type 2 diabetes mellitus and obesity.With the further study,it is found that resistin is closely related to cardiovascular diseases such as coronary heart disease,myocardial hypertrophy,heart failure and so on.Protein tyrosine kinase / signal transducer and activator of transcription(JAK/STAT)signal pathway is an indispensable pathway to muscle cell proliferation and differentiation,studies have shown that the JAK/STAT signaling pathway have great relevance with myocardial hypertrophy and heart failure.ObjectivesThrough resistin inducing H9c2 cardiomyocyte hypertrophy model,Discussion the effect of JAK2/STAT3 signaling pathway in resistin induced H9C2 cardiomyocytes hypertrophy and its possible molecular mechanisms,explore the new methods of effective prevention and treatment of cardiomyocyte hypertrophy so as to provide new ways for the clinical treatment of myocardial hypertrophy and heart failure.MethodsThe synchronized grow H9C2 myocardial cells were selected and divided into control group,resistin group,resistin+Ag490 group and Ag490 group.The myocardial cells in control group were cultured with low blood serum medium;the myocardial cells in resistin group were cultured with low blood serum medium which contained 50 ?g.L-1 resistin;the myocardial cells in resistin+Ag490 group were first cultured with low blood serum medium which contained 100 ?mol Ag490,then were cultured with low blood serum medium which contained 50 ?g.L-1 resistin;the myocardial cells in Ag490 group were cultured with low blood serum medium which contained 100 ?mol Ag490.After culturing in appropriate intervention conditions.The surface area picture element of myocardial cells were measured by ImageJ software;the content of protein was measured by bicinchoninic acid(BCA)method;the relative expression levels of alpha smooth muscle aorta(?-SMA),C-MYC,phosphorylated janus kinase 2(P-JAK2),phosphorylated transducer and activator of transcription 3(P-STAT3)were measured by Western Blot.Measurement data were expressed by mean + standard deviation(±s),and ANOVA variance analysis were used among each groups,when P<0.05,the difference was statistically significant.ResultsThe surface area picture element of myocardial cells and protein content of single cell in resistin group were significantly greater than those in the control group,resistin+Ag490 group and Ag490 group(P<0.05);the surface area picture element of myocardial cells and protein content of single cell in resistin+Ag490 group were significantly greater than those in the control group and Ag490 group(P>0.05);there were no statistic difference in the surface area picture element of myocardial cells and protein content of single cell between the control group and Ag490 group(P<0.05).The expression of ?-SMA protein in myocardial cells in resistin group was significanlty higher than that in the control group,resistin+Ag490 group and Ag490 group(P<0.05);there was no statistic difference in the expression of ?-SMA protein in myocardial cells among other groups(P>0.05).The expression of C-MYC protein in myocardial cells in resistin group was significanlty higher than that in the control group,resistin+Ag490 group and Ag490 group(P<0.05);the expression of C-MYC protein in myocardial cells in resistin+Ag490 group was significanlty higher than that in the control group(P<0.05);there was no statistic difference in the expression of C-MYC protein in myocardial cells among other groups(P>0.05).The expression level of P-JAK2 and P-STAT3 protein in myocardial cells in resistin group was significanlty higher than that in the control group,resistin+Ag490 group and Ag490 group(P<0.05);there was no statistic difference in the expression level of P-JAK2 and P-STAT3 protein in myocardial cells among other groups(P>0.05)ConclusionsResistin can induce H9C2 cardiomyocytes hypertrophy;JAK2 / STAT3 signaling pathways play a role in the process of resistin induced myocardial hypertrophy.