scholarly journals Differential gene expression for glutamic acid decarboxylase and type II calcium-calmodulin-dependent protein kinase in basal ganglia, thalamus, and hypothalamus of the monkey

1991 ◽  
Vol 11 (6) ◽  
pp. 1540-1564 ◽  
Author(s):  
DL Benson ◽  
PJ Isackson ◽  
SH Hendry ◽  
EG Jones
Keyword(s):  
Gene Expression ◽  
Basal Ganglia ◽  
Protein Kinase ◽  
Glutamic Acid Decarboxylase ◽  
Acid Decarboxylase ◽  
Type Ii ◽  
Dependent Protein Kinase ◽  
Calcium Calmodulin Dependent ◽  
Dependent Protein ◽  
Differential Gene

P6344Volume overload-triggered pathological myocardial remodeling occurs in the absence of calcium/calmodulin-dependent protein kinase type II delta

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Elkenani ◽  
B A Mohamed ◽  
E Buchholz ◽  
D Lbik ◽  
M Schnelle ◽  
...  
Keyword(s):  
Heart Failure ◽  
Protein Kinase ◽  
Heart Weight ◽  
Type Ii ◽  
Myocardial Remodeling ◽  
Dependent Protein Kinase ◽  
Mortality Pattern ◽  
Calcium Calmodulin Dependent ◽  
Dependent Protein ◽  
The Impact

Abstract Background Calcium/calmodulin-dependent protein kinase type II delta (CamKIIδ), the predominant cardiac CaMKII isoform, has been implicated in the progression of myocardial infarction- and pressure overload-induced pathological remodeling and heart failure, but its role in volume overload (VO) has not been defined. We have previously reported an activation of CamKII during transition to HF in VO. Purpose Here, we analyzed the impact of CamKIIδ deletion in VO-triggered myocardial remodeling and heart failure development. Methods CaMKIIδ knockout (CaMKIIδ-KO) and wild-type (WT) littermates were exposed to aorto-caval shunt-induced VO, and the progression of myocardial remodeling was assessed by serial echocardiography, histological and molecular analyses. Results CaMKIIδ-KO and WT littermates exhibited similar mortality pattern in response to VO. Serial echocardiographic measurements showed a comparable eccentric myocardial remodeling, altered left ventricle geometry and perturbed ventricular function after shunt. At 12 weeks post-shunt both CaMKIIδ-KO and WT mice experienced comparable increases in relative heart weight, cardiomyocyte diameter, cardiac apoptosis, and hypertrophic genes expression. Conclusion We therefore conclude that CaMKIIδ signaling is dispensable for the progression of pathological cardiac remodeling induced by VO. This should be considered before CaMKII inhibition is approved therapeutically for HF treatment.

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