Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P20020 (
adenosine triphosphatase
)
3,299
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Hypothyroidism is associated with profound left ventricular dysfunction. Triiodothyronine (T
3
) supplementation may improve cardiac function after ischemic reperfusion (I/R) injury. In the present study, the effect of T
3
on major calcium cycling proteins and high-energy phosphate content during I/R was evaluated. Isolated perfused rat hearts were divided into 5 groups: Sham Control (Sham, n=10), Control (n=8), T
3
10 nM (T
3
-10, n=10), T
3
25 nM (T
3
-25, n=10) and T
3
50 nM (T
3
-50, n=10). T
3
was administrated for 60 min before 30 min of ischemia and 120 min of reperfusion. The protein contents of Ca
2+
-release channels (RyR2), Ca
2+
-
adenosine triphosphatase
(SERCA2a), phospholamban (PLB), sarcolemmal Ca
2+
-
adenosine triphosphatase
(PMCA) and sodium-calcium exchanger (NCX), as well as the high-energy phosphate content in heart tissues were measured by western blot analysis. The results revealed that T
3
improved the contractile recovery (left ventricular developed pressure; +dP/dt, -dP/dt) after I/R. Western blotting assays demonstrated that I/R depressed the contents of
RYR2
, SERCA2a and phosphorylated
RYR2
and PLB; there were no effects on the contents of PLB, PMCA and NCX. T
3
reversed I/R-induced degradation of RyR2 and SERCA2a, restored the phosphorylation of RyR2 and PLB, and preserved the high-energy phosphate contents of ATP and creatine phosphate. T
3
supplementation protected the heart against I/R injury via the preservation of Ca
2+
-cycling proteins and high-energy phosphate content.
...
PMID:Cardioprotective effects of triiodothyronine supplementation against ischemia reperfusion injury by preserving calcium cycling proteins in isolated rat hearts. 3179 15
