scholarly journals Abnormalities of Calcium Handling Proteins in Skeletal Muscle Mirror Those of the Heart in Humans With Heart Failure: A Shared Mechanism?

2012 ◽  
Vol 18 (9) ◽  
pp. 724-733 ◽  
Author(s):  
Holly R. Middlekauff ◽  
Chris Vigna ◽  
M. Anthony Verity ◽  
Gregg C. Fonarow ◽  
Tamara B. Horwich ◽  
...  
2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Yao Wu ◽  
Feifei Si ◽  
Xiaojuan Ji ◽  
Kunfeng Jiang ◽  
Sijie Song ◽  
...  

Background. This study was undertaken to determine relative contributions of phosphorylation and oxidation to the increased activity of calcium/calmodulin-stimulated protein kinase II (CaMKII) in juveniles with cardiac myocyte dysfunction due to increased pressure overload. Methods. Juvenile rats underwent abdominal aortic constriction to induce heart failure. Four weeks after surgery, rats were then randomly divided into two groups: one group given valsartan (HF + Val) and the other group given placebo (HF + PBO). Simultaneously, the sham-operated rats were randomly given valsartan (Sham + Val) or placebo (Sham + PBO). After 4 weeks of treatment, Western blot analysis was employed to quantify CaMKII and relative calcium handling proteins (RyR2 and PLN) in all groups. Results. The deteriorated cardiac function was reversed by valsartan treatment. In ventricular muscle cells of group HF + PBO, Thr287 phosphorylation of CaMKII and S2808 phosphorylation of RyR2 and PLN were increased and S16 phosphorylation of PLN was decreased compared to the other groups, while Met281 oxidation was not significantly elevated. In addition, these changes in the expression of calcium handling proteins were ameliorated by valsartan administration. Conclusions. The phosphorylation of Thr286 is associated with the early activation of CaMKII rather than the oxidation of Met281.


2010 ◽  
Vol 42 (5) ◽  
pp. 847-855 ◽  
Author(s):  
MORTEN MUNKVIK ◽  
TOMMY A. REHN ◽  
GUNNAR SLETTALØKKEN ◽  
ALMIRA HASIC ◽  
JOSTEIN HALLÉN ◽  
...  

2002 ◽  
Vol 92 (4) ◽  
pp. 1524-1530 ◽  
Author(s):  
Lu Lu ◽  
Dan Feng Mei ◽  
An-Guo Gu ◽  
Su Wang ◽  
Benjamin Lentzner ◽  
...  

The cardiac sarcoplasmic reticulum calcium-ATPase (SERCA2a), Na+/Ca2+ exchanger (NCX1), and ryanodine receptor (RyR2) are proteins involved in the regulation of myocyte calcium. We tested whether exercise training (ET) alters those proteins during development of chronic heart failure (CHF). Ten dogs were chronically instrumented to permit hemodynamic measurements. Five dogs underwent 4 wk of cardiac pacing (210 beats/min for 3 wk and 240 beats/min for the 4th wk), whereas five dogs underwent the same pacing regimen plus daily ET (5.1 ± 0.3 km/h, 2 h/day). Paced animals developed CHF characterized by hemodynamic abnormalities and reduced ejection fraction. ET preserved resting hemodynamics and ejection fraction. Left ventricular samples were obtained from all dogs and another five normal dogs for mRNA (Northern analysis, band intensities normalized to glyceraldehyde-3-phosphate dehydrogenase) and protein level (Western analysis, band intensities normalized to tubulin) measurements. In failing hearts, SERCA2a was decreased by 33% ( P < 0.05) and 65% ( P < 0.05) in mRNA and protein level, respectively, compared with normal hearts; there was only an 8.6% reduction in mRNA and a 32% reduction in protein in exercised animals ( P < 0.05 from CHF). mRNA expression of NCX1 increased by 44% in paced-only dogs compared with normal ( P < 0.05) but only by 22% in trained dogs ( P < 0.05 vs. CHF); protein level of NCX1 was elevated in paced-only dogs (71%, P < 0.05) but partially normalized by ET (33%, P < 0.05 from CHF). RyR2 was not altered in any of the dogs. In conclusion, long-term ET may ameliorate cardiac deterioration during development of CHF, in part via normalization of myocardial calcium-handling proteins.


2014 ◽  
Vol 7 (6) ◽  
pp. 976-985 ◽  
Author(s):  
Komei Tanaka ◽  
Richard M. Wilson ◽  
Eric E. Essick ◽  
Jennifer L. Duffen ◽  
Philipp E. Scherer ◽  
...  

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