Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
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Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: EC:2.3.3.1 (
citrate synthase
)
4,488
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
To investigate the effect of exercise training on calcium movements by isolated cardiac sarcoplasmic reticulum (SR), mongrel dogs either remained sedentary (S) or were exercise-trained (E) via running for a period of 8-10 wk. The trained state was confirmed by the increase in skeletal muscle
citrate synthase
activity and decreases in submaximal exercise heart rates in the E group but not in the S dogs. The properties of isolated cardiac SR were identical between the groups. The variables tested included ATP-dependent calcium transport and calcium-stimulated ATPase activity. Importantly, there was no difference in spontaneous calcium release which occurred after peak ATP-dependent calcium accumulation was reached. Calcium release from passively loaded vesicles induced by calcium and ionophore also did not differ in the SR isolated from the E dogs. The change in the affinity of the SR Ca ATPase for calcium after the addition of the polyanion, heparin, was similar in both groups, indicating that the regulation of calcium-stimulated ATPase activity by the SR protein,
phospholamban
, is not modified by exercise training. We conclude that exercise training of 8-10 wk duration does not alter the calcium handling properties of cardiac SR isolated from mongrel dogs.
...
PMID:Canine cardiac sarcoplasmic reticulum is not altered with endurance exercise training. 828 11
Hypothyroidism (Hypo) is a risk factor for cardiovascular diseases, including heart failure. Hypo rapidly induces Ca
2+
mishandling and contractile dysfunction (CD), as well as atrophy and ventricular myocytes (VM) remodeling. Hypo decreases SERCA-to-
phospholamban
ratio (SERCA/PLB), and thereby contributes to CD. Nevertheless, detailed spatial and temporal Ca
2+
cycling characterization in VM is missing, and contribution of other structural and functional changes to the mechanism underlying Ca
2+
mishandling and CD, as transverse tubules (T-T) remodeling, mitochondrial density (D
mit
) and energy availability, is unclear. Therefore, in a rat model of Hypo, we aimed to characterize systolic and diastolic Ca
2+
signaling, T-T remodeling, D
mit
,
citrate synthase
(CS) activity and high-energy phosphate metabolites (ATP and phosphocreatine). We confirmed a decrease in SERCA/PLB (59%), which slowed SERCA activity (48%), reduced SR Ca
2+
(19%) and blunted Ca
2+
transient amplitude (41%). Moreover, assessing the rate of SR Ca
2+
release (dRel/dt), we found that early and maximum dRel/dt decreased, and this correlated with staggered Ca
2+
transients. However, dRel/dt persisted during Ca
2+
transient relaxation due to abundant late Ca
2+
sparks. Isoproterenol significantly up-regulated systolic Ca
2+
cycling. T-T were unchanged, hence, cannot explain staggered Ca
2+
transients and altered dRel/dt. Therefore, we suggest that these might be caused by RyR2 clusters desynchronization, due to diminished Ca
2+
-dependent sensitivity of RyR2, which also caused a decrease in diastolic SR Ca
2+
leak. Furthermore, D
mit
was unchanged and CS activity slightly decreased (14%), however, the ratio phosphocreatine/ATP did not change, therefore, energy deficiency cannot account for Ca
2+
and contractility dysregulation. We conclude that decreased SR Ca
2+
, due to slower SERCA, disrupts systolic RyR2 synchronization, and this underlies CD.
...
PMID:Underlying mechanism of the contractile dysfunction in atrophied ventricular myocytes from a murine model of hypothyroidism. 2974 31
