Dissertation
Dissertation > Medicine, health > Internal Medicine > Heart, blood vessels ( circulatory ) disease > Heart disease

Ca~(2+) /calmodulin-dependent Protein Kinaseⅱdirectly Mediates Angiotensin Ⅱ-induced Cardiac Remodeling

Author LiuShanHong
Tutor LiJingDong
School Huazhong University of Science and Technology
Course Internal Medicine
Keywords Cardiac remodeling Cardiac hypertrophy Myocardial fibrosis Angiotensin Ⅱ CaMK Ⅱ
CLC R541
Type Master's thesis
Year 2010
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Purpose : Angiotensin Ⅱ (Ang Ⅱ) mice induced myocardial hypertrophy, myocardial fibrosis model , excited to explore the renin - angiotensin - aldosterone system (RAAS) induced cardiac remodeling process calcium / calmodulin -dependent protein kinase II (CaMK Ⅱ) changes in the characteristics . Methods: Male C57BL/6J mice were randomly divided into Ang Ⅱ group and the control group ( n = 10 ) . Both groups was 1.6 mg / (kg.d) dose intraperitoneal injection of Ang Ⅱ and distilled water three weeks , the observation of modeling three weeks after the two groups of animals of cardiac hypertrophy , fibrosis and CaMK Ⅱ change characteristics . Early body weight (IBW) and final body weight (FBW) , heart weight (HW) and heart weight and body weight ratio (HW / BW) quantitative myocardial hypertrophy ; hematoxylin prime - eosin and Masson staining , respectively, observed two groups of animals left ventricular myocardial cells inside diameter size and myocardial fibrosis ; using real-time quantitative PCR CaMK Ⅱ gene expression level ; Western blot analysis of the content and activity of CaMK Ⅱ change . Results : in Ang Ⅱ group 3 weeks after myocardial hypertrophy , cardiac myocyte transverse diameter , myocardial fibrosis [ myocardial perivascular collagen area (PVF) / vessel lumen area (VA)] were significantly higher , respectively, in the control group 1.08 1.57 and 2.3 times the differences were statistically significant ( P lt; 0.05 ) ; Ang II group CaMK Ⅱ of the level of gene expression , protein content and activity of the control group were significantly increased control group 1.53,2.03 and 2.94 , respectively times , the differences were statistically significant ( P lt; 0.05 ) . Conclusion: intraperitoneal injection of certain doses of Ang Ⅱ can significantly increase cardiac CaMK Ⅱ of expression and induced cardiac hypertrophy and fibrosis , suggesting that RAAS excitement caused by heart refactoring process CaMK Ⅱ is a direct referral guide Ang Ⅱ effect of extracellular important signal transduction factor .

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