ABSTRACT
Objective To explore the effect and mechanism of protein kinase N1(PKN1)on the proliferation of mouse cardiomyocytes.Methods Two 1-day-old mice were anesthetized with isoflurane,and their cardiomyocytes were isolated and divided into the control group and the interference group.The cardiomyocytes in the interference group were transfected with PKN1 fragments,while the cardiomyocytes in the control group were transfected with control fragments.According to the random number table method,10 mice were divided into the normal group and the observation group,with 5 mice in each group.The mice in the observation group were injected with PKN1 adenovirus in situ in the heart,while the mice in the normal group were injected with empty adenovirus in situ in the heart.The Ki-67 positive expression in myocardial cells and tissues of mice in the four groups was detected by immunofluorescence assay,indicating the proliferation ability of cardiomyocytes.The PKN1 mRNA expression in cardiomyocytes of mice in the control group and interference group was measured by real-time fluorescence quan-titative polymerase chain reaction.The expression of PKN1 and cyclin D1 proteins in cardiomyocytes of mice in the control group and interference group was determined by Western blot.Results The positive expression rates of Ki-67 in myocardial cells of mice in the interference group was significantly lower than that in the control group(t=11.201,P＜0.01);the positive expression rate of Ki-67 in myocardial tissue of mice in the observation group was significantly lower than that in the normal group(t=11.851,P＜0.01).The relative expression level of PKN1 mRNA in cardiomyocytes of mice in the interference group was significantly lower than that in the control group(t=7.022,P＜0.01).The relative expression levels of PKN1 and cyclin D1 proteins in cardiomyocytes of mice in the interference group were significantly lower than those in the control group(t=5.762,6.884;P＜0.01).Conclusion The decreased expression of PKN1 in mouse cardiomyocytes can inhibit the expression of cyclin D1 protein,thereby restraining cardiomyocyte proliferation.
ABSTRACT
Objective To investigate the correlation between myocardial fibrosis evaluated by cardiac magnetic resonance (CMR)T1 mapping and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in elderly patients with ischemic cardiomyopathy (ICM).Methods The 56 hospitalized patients with ICM(ICM group)and 20 healthy volunteers(control group)were recruited in cardiology department of Henan Provincial People's Hospital from April 2014 to June 2017.Clinical data,serum NT-proBNP detection,CMR T1 mapping and contrast-enhanced scan were determined,retrospectively collected and compared between two groups.The differences in myocardial extracellular volume fraction(ECVF)and NT-proBNP levels were compared among the control group,the ICM group and the ICM subgroups with different degree of cardiac dysfunction.The correlation between ECVF and NT-proBNP level was analyzed.Results The levels of ECVF and NT-proBNP were significantly higher in ICM group than in control group[(35.1t6.2)％ vs.(25.3±2.2)％ for ECVF,and(3 902.7± 1 670.3)ng/L vs.(280.5± 140.5)ng/L for NT-proBNP,t =6.917 and 9.645 respectively,both P＜0.01].Along with NYHA Functional Class upgrade of Ⅱ to Ⅲ] to Ⅳ of the ICM subgroups,the levels of ECVF and NT-proBNP were significantly increased (F =18.372 for ECVF,61.82 for NT-proBNP,all P＜0.01).There was a positive correlation between ECVF and NT-proBNP level in ICM patients (r =0.666,P ＜ 0.05).Conclusions Serum NT-proBNP level is correlated with the degree of myocardial fibrosis,which might be used as an indicator of myocardial fibrosis in ICM patients.