ABSTRACT
Objective: To investigate the influence of intermittent cold stress on collagen content of atherosclerotic plaque in experimental ApoE-/-mice. Methods: A total of 20 male ApoE-/-mice at 8 weeks of age were divided into 2 groups:Experimental group, the mice had intermittent cold exposure at (4 ± 1)°C from 8am to 12noon and Control group, the mice were living at (24 ± 2) °C. All animals were treated for 12 weeks, n=10 in each group. The collagen content of atherosclerotic plaque at the aortic root in ApoE-/-mice was observed by Masson staining, the protein expressions of aortic MMP-2, MMP-9 and TIMP-1 were examined by Western blot analysis. Results: Compared with Control group, the Experimental group presented the lower collagen content of atherosclerotic plaque at the aortic root, higher protein expressions of MMP-2, MMP-9 and lower protein expression of TIMI 1. Conclusion: Intermittent cold stress may disturb the balance of MMP/TIMP and decrease collagen content of atherosclerotic plaque to form vulnerable plaque in experimental ApoE-/-mice which may cause acute coronary syndrome.
ABSTRACT
Objective To investigate the involvement of mitogen-activated protein kinase(MAPK)and PI3K(phosphatidylinositol 3 kinase)/ Protein kinase B(Akt) signal transduction pathways in the mechanism of myocardium remodeling in patients with congestive heart failure(CHF).Methods Thirty nine patients of mitral valve disease with CHF were randomly selected and 30 cases of healthy persons were included as controls.Cardiac function parameters were measured by echocardiography.Concentration of AngⅡ in plasma and myocardial tissues was determined by radio immunoassay.Activity of PKC was determined by using competive prote in binding method,activity of MAPK was detected by the methods of immunoprecitipation.Immunoprecitipation was used to assay the protein expression and phosphorylation of PI3K and Akt(Protein kinase B),protein expression of C-FOS and ?-skeletal-actin in myocardial tissues.Results Pathological changes of myocardial tissues in CHF with valvular heart diseaseshowed typical myocardial remodeling.The hypertrophy was dominant at early stagy of CHF,while at end stage the characteristics include disordered alignament of the myocytes,the discontinuity and dissolving of cardiomyofibrills,destroyed subcellular organs,and the hyperplasia of interstitial tissue.AngⅡ concentration in plasm and myocardial tissues in patients with CHF was higher than those in the control group(P
ABSTRACT
Objective To investigate the involvement of mitogen-activated protein kinase(MAPK)system and hypertrophy related genes in myocardial remodeling mechanism of patients with congestive heart failure(CHF).Methods Thirty-nine patients of mitral valve disease with CHF were randomly selected and 30 cases of healthy persons were included as controls.Cardiac function parameters were measured by echocardiography.Concentration of AngⅡ in plasma and myocardial tissues were determined by radio immunoassay.Immunoprecipitation was used to assay the protein expression and phosphorylation of c-jun NH2-terminal kinase(JNK),extracellular signal regulated kinase(ERK),P 38- mitogen-activated protein kinase(P 38-MAPK)in myocardial tissues;protein expression of c-myc,c-myb,c-jun was also determined by immunoprecipitation.Results Compared to the control group,the phosphorylation of ERK1/2 was obvious in heart function class Ⅱ group(P0.05);phosphorylation of JNK was obvious in CHF groups(P0.05);there was no expression in control group.Conclusion MAPK activated by renin angiotensin system may play an important role by causing the protein expression of c-myc,c-myb,c-jun in myocardial remodeling in patients with CHF.