Assessment of cardiac structure and function by echocardiographic values for male Balb/c mice / 中国应用生理学杂志

<p><b>AIM</b>To assess the parameters of cardiac structure and function of male Balb/c mice by the echocardiography.</p><p><b>METHODS</b>A total of 27 male Balb/c mice (from five to seven week old) were examined with a 13-MHz transthoracic linear-array transducer, hearts were removed from mice anesthetized with Nembutal, and the left ventricular (LV) mass were weighed.</p><p><b>RESULTS</b>Complete 2-dimensional echocardiography for cardiac structure and function were obtained. Hemodynamic parameters were recorded. A correlation existed between LV weight (x) and echocardiographic LV mass (y) with the 2D) guided M-mode method: y = 1.15x + 3.26, (r = 0.80).</p><p><b>CONCLUSION</b>Echocardiography appears to be a promising approach for noninvasively assessing LV mass and function in mice.</p>

Association between cardiac troponin I phosphorylation/degradation and cardiomyopathies / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the association between cTnI phosphorylation/degradation and cardiomyopathies in extransplanted myocardium.</p><p><b>METHODS</b>cTnI phosphorylation and degradation as well as PKC (beta1, beta2) expressions were determined in extransplanted hearts from patients with cardiomyopathies (n = 8) and from traffic accidents (n = 6) by Western blot.</p><p><b>RESULTS</b>The cTnI bands were observed in LV myocardium of cardiomyopathy patients and normal myocardium while and cTnI degradation bands were only detected in LV myocardium from patients with cardiomyopathies. The phosphorylated cTnI bands were significantly upregulated in LV myocardium of cardiomyopathy patients compared to normal myocardium (P < 0.05). There was no myocardial PKCbeta1, PKCbeta2 expression in all examined hearts.</p><p><b>CONCLUSION</b>The cTnI degradation products and increased phosphorylated cTnI expression are likely involved in the pathogenesis and development of cardiomyopathy.</p>

Reduced Ca2+ current in rat cardiomyocytes transfected with troponin I R145W mutation gene / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effects of cardiac troponin I R145W mutation, detected in Chinese patients with hypertrophic cardiomyopathy, on Ca(2+) current modulation.</p><p><b>METHODS</b>R146W mutation (resemble R145W in human) was introduced into rat cardiac troponin I cDNA by site-directed mutagenesis. With EGFP as a reporter gene, replication-defective adenovirus containing the wild or mutant cTnI gene was constructed. Adult rat cardiomyocytes, were isolated by Langendorff perfusion and cultured with serum-free medium and transduced with the recombinant adenoviruses. Western blot was used to determine the recombinant proteins. Whole cell patch clamp was employed to record L-type Ca(2+) currents on cultured myocytes. Intracellular free Ca(2+) and caffeine-induced sarcoplasmic reticulum (SR) Ca(2+) release were determined after the cells incubated with Fura-2/AM.</p><p><b>RESULTS</b>DNA sequencing confirmed that R146W mutation was generated in rat cTnI cDNA. Bright green fluorescence was observed in the cultured cardiomyocytes at 48 h after transduction. The recombinant proteins could be identified with cTnI or GFP monoclonal antibody. The peak current of L-type Ca(2+) channel in cells transduced with cTnI R146W was significantly decreased compared to control cells and cells transfected with wild cTnI. Intracellular free Ca(2+) concentrations and caffeine-induced SR Ca(2+) release determined by Fura-2/AM were similar among various cells.</p><p><b>CONCLUSION</b>Reduced peak current of L-type Ca(2+) channel in cells transduced with cTnI R146W might contribute to the disease-causing mechanism of this mutation in patients with hypertrophic cardiomyopathy.</p>

Role of calcineurin in the progression of cardiac hypertrophy in renovascular hypertensive rats / 生理学报

The present study was to investigate the mRNA, protein expression and the activity of calcineurin in the hypertrophic heart, and to determine the effect of calcineurin inhibitor--cyclosporine A (CsA) on the regression of cardiac hypertrophy in renovascular hypertensive rats. Renovascular hypertension was induced by two kidney-one clip methods. Two months after the operation, cardiac hypertrophy was determined by histological analysis performed in some rats (2K1C-2M), then the rats were subdivided into 2 groups: (1) 3-month old two kidney-one clip group (2K1C-3M) with rats receiving 0.9% NaCl per day for one month, and (2) CsA-treated group with rats treated with CsA for one month. Sham-operated rats were used as control. The ratio of the left ventricular weight to tibial length (LVW/TL), the area of cardiac myocyte, mRNA and protein expression and the activity of calcineurin were determined. Both the LVW/TL and the cardiomyocyte area were significantly larger in 2K1C-2M and 2K1C-3M rats than in age-matched sham-operated rats. Treatment with CsA significantly attenuated the increase in the LVW/TL as well as the cardiomyocyte area. The mRNA, protein expression and the activity of calcineurin were significantly higher in 2K1C-2M and 2K1C-3M rats than those in the age-matched sham-operated rats, while the elevation of mRNA, protein expression and activity of calcineurin were significantly suppressed in the CsA-treated rats. In conclusion, calcineurin plays a role in the progression of cardiac hypertrophy in renovascular hypertensive rats. The inhibition of calcineurin can reverse cardiac hypertrophy.