Calcium handling proteins in the failing human heart

1997 ◽  
Vol 92 (S1) ◽  
pp. 87-93 ◽  
Author(s):  
G. Hasenfuss ◽  
M. Meyer ◽  
W. Schillinger ◽  
M. Preuss ◽  
B. Pieske ◽  
...  
Keyword(s):  
Human Heart ◽  
Calcium Handling ◽  
Calcium Handling Proteins

Calcium handling proteins in the failing human heart

1998 ◽  
pp. 141-151
Author(s):  
G. Hasenfuss ◽  
M. Meyer ◽  
W. Schillinger ◽  
M. Preuss ◽  
B. Pieske ◽  
...  
Keyword(s):  
Human Heart ◽  
Calcium Handling ◽  
Calcium Handling Proteins

Chamber-specific changes in calcium-handling proteins in the type 2 diabetic human heart with preserved ejection fraction

2015 ◽  
Vol 193 ◽  
pp. 53-55 ◽  
Author(s):  
Carol T. Bussey ◽  
Gillian Hughes ◽  
Pankaj Saxena ◽  
Ivor F. Galvin ◽  
Richard W. Bunton ◽  
...  
Keyword(s):  
Ejection Fraction ◽  
Human Heart ◽  
Calcium Handling ◽  
Preserved Ejection Fraction ◽  
Calcium Handling Proteins ◽  
Type 2 Diabetic

scholarly journals Allied Professionals7Screening for eligibility for subcutaneous icd implant in adults with congenital heart disease: how many patients are eligible?8Identifying the outcome of patients in a multispeciality nurse led rapid access blackout clinic undergoing implantable loop recorders for unexplained syncope9Implant of medtronic linq in an outpatient setting10Does time from diagnosis of atrial fibrillation to ablation effect success of catheter ablation?11Detection and management of atrial fibrillation in the pacing clinic12The efficacy of a nurse-led cardioversion service on clinical outcomes13Do major ion channels of pacemaker clock also play a role in atrioventricular nodal conduction in young and aged rats?14Anatomical and functional determinants of preferential rotor locations and stability in atrial fibrillation15Pacemaker-induced cardiomyopathy in the sheep: rva but not rvot pacing results in a heart failure cellular phenotype16A steep apd-restitution slope does not cause apd-alternans in the intact human heart17Cardiac sites of the in-vivo human heart exhibiting apd-alternans show changes in calcium-handling proteins and repolarizing currents18Dynamic transmural activation recovery interval gradients exceed apico-basal gradients in the intact human heart: Table

EP Europace ◽  
2015 ◽  
Vol 17 (suppl 5) ◽  
pp. v3-v5 ◽  
Author(s):  
S. Cunningham ◽  
A. Hall ◽  
A.J. Jackson ◽  
L.J.S. Jarrett-Smith ◽  
P.A. Rees ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Human Heart ◽  
Calcium Handling ◽  
Aged Rats ◽  
Subcutaneous Icd ◽  
Recovery Interval ◽  
Atrioventricular Nodal Conduction ◽  
Implantable Loop Recorders ◽  
Calcium Handling Proteins

scholarly journals Cardiac Protection of Valsartan on Juvenile Rats with Heart Failure by Inhibiting Activity of CaMKII via Attenuating Phosphorylation

2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Yao Wu ◽  
Feifei Si ◽  
Xiaojuan Ji ◽  
Kunfeng Jiang ◽  
Sijie Song ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Myocyte ◽  
Pressure Overload ◽  
The Other ◽  
Calcium Handling ◽  
Juvenile Rats ◽  
Abdominal Aortic ◽  
Calcium Handling Proteins ◽  
Increased Activity ◽  
Induce Heart Failure

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.

Pressure Overload-Induced Heart Failure Is Associated With an Increased Enzymatic O-GlcNAcylation of Calcium Handling Proteins

2010 ◽  
Vol 16 (8) ◽  
pp. S12
Author(s):  
Jorge Suarez ◽  
Mary O. Oyeleye ◽  
Wenlong Han ◽  
Wolfgang H. Dillmann
Keyword(s):  
Heart Failure ◽  
Pressure Overload ◽  
Calcium Handling ◽  
Calcium Handling Proteins

P943The effects of ovariectomy on guinea pig cardiomyocyte intracellular calcium regulation and phosphorylation

EP Europace ◽  
2020 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
E Ching ◽  
J M Firth ◽  
A J Francis ◽  
N Islam ◽  
K T Macleod
Keyword(s):  
Intracellular Calcium ◽  
Calcium Regulation ◽  
Left Ventricular ◽  
Calcium Handling ◽  
Time To Peak ◽  
Oestrogen Deficiency ◽  
Calcium Handling Proteins ◽  
Presence And Absence ◽  
Intracellular Calcium Regulation

Abstract Background Differences in cardiovascular disease risk between men and women have been partly attributed to the cardioprotective effects of oestrogen. Long-term oestrogen deficiency has been shown to alter cardiomyocyte intracellular calcium handling, but little is known about the mechanisms by which these changes occur. Oestrogen is thought to induce both genomic and non-genomic effects on cardiomyocytes, the latter including phosphorylation of calcium handling proteins. Purpose This study addresses the hypothesis that long-term oestrogen deficiency increases protein kinase A (PKA) and calcium/calmodulin-dependent kinase II (CaMKII) phosphorylation in cardiomyocytes, resulting in altered intracellular calcium regulation. Methods Female guinea pigs underwent sham (n = 7) or ovariectomy (OVx) (n = 8) operations and 150 days later, left ventricular myocytes were enzymatically isolated and loaded with fluo-4AM to monitor intracellular calcium. Calcium transients (CaT) were recorded using confocal microscopy. PKA and CaMKII phosphorylation were inhibited by superfusing cells with specific inhibitors, PKI and AIP, respectively. Experiments were carried out both in the presence and absence of β-agonist, isoprenaline (ISO), and relative changes to CaT parameters compared between OVx and sham cells. Results CaT amplitude was greater (p < 0.05) in the OVx group (ΔF/Fo= 2.51 ± 0.57) compared with sham (ΔF/Fo = 2.16 ± 0.57). Inhibition of CaMKII phosphorylation increased CaT amplitude in the sham but not OVx group, both in the presence (by 22%, p < 0.01) and absence of ISO (by 19%, p < 0.01). Time to peak of the CaT increased to a greater extent following inhibition of PKA and CaMKII phosphorylation in the OVx group compared with sham, both in the presence (by 69%, p < 0.0001) and absence (by 162%, p < 0.0001) of ISO respectively. CaT decay time significantly increased (by 21%, p < 0.01) in the sham group following inhibition of PKA and CaMKII together, whilst decay times in the OVx group remained unchanged in the presence and absence of ISO. At higher pacing rates, time to peak of the CaT decreased significantly (by 48%, p < 0.01) in the OVx group but not sham with inhibition of phosphorylation. Conclusion Our findings suggest ovariectomy alters intracellular calcium regulation and some of these effects appear to be mediated by alterations in phosphorylation of calcium handling proteins and/or changes to sites of phosphorylation.

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