Cardiac sarcoplasmic reticulum Ca(2+)-ATPase expression in streptozotocin-induced diabetic rat heart.
Chronic diabetes due to streptozotocin administration has been shown to induce heart dysfunction characterized by prolonged relaxation time as well as decreased Ca2+ transport and Ca(2+)-ATPase (SERCA2) activities of the cardiac sarcoplasmic reticulum (SR). Rats made diabetic with 65 mg/kg of streptozotocin for 3 and 5 weeks exhibited decreased SR Ca(2+)-pump activities; these were normalized upon treatment with insulin. Northern blot and slot blot analyses did not show statistically significant reduction in the relative level of SERCA2 mRNA expression in diabetic or insulin treated rats. Quantitation of SERCA2 protein by Western blot did not reveal any change in diabetic and insulin treated animals. These results suggest that the defect in SR Ca(2+)-pump may not be due to changes at the transcriptional or translational levels in the diabetic heart.
Zarain-Herzberg
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Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba, Canada.
Yano
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K
Elimban
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Dhalla
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D000818:Animals; D015153:Blotting, Western; D000252:Calcium-Transporting ATPases / Q000096:biosynthesis* / Q000302:isolation & purification; D018076:DNA, Complementary; D003921:Diabetes Mellitus, Experimental / Q000201:enzymology*; D015870:Gene Expression / Q000187:drug effects; D006352:Heart Ventricles; D007328:Insulin / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D008565:Membrane Proteins / Q000096:biosynthesis / Q000302:isolation & purification; D009206:Myocardium / Q000201:enzymology*; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012519:Sarcoplasmic Reticulum / Q000201:enzymology*
D018076:DNA, Complementary; D007328:Insulin; D008565:Membrane Proteins; D012333:RNA, Messenger; D000252:Calcium-Transporting ATPases