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Am J Physiol Endocrinol Metab 284: E366-E376, 2003; doi:10.1152/ajpendo.00254.2002
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Vol. 284, Issue 2, E366-E376, February 2003

Impaired cardiac function and IGF-I response in myocytes from calmodulin-diabetic mice: role of Akt and RhoA

Jinhong Duan1, Hai-Ying Zhang1, Steven D. Adkins1, Bonnie H. Ren1, Faye L. Norby1, Xiaochun Zhang1, Joseph N. Benoit1, Paul N. Epstein2, and Jun Ren1

1 Department of Pharmacology, Physiology, and Therapeutics, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota 58203; and 2 Department of Pediatrics, University of Louisville School of Medicine, Louisville, Kentucky 40202

This study characterized the cardiac contractile function and IGF-I response in a transgenic diabetic mouse model. Mechanical properties were evaluated in cardiac myocytes from OVE26 diabetic and FVB wild-type mice, including peak shortening (PS), time to PS (TPS), time to 90% relengthening (TR90) and maximal velocity of shortening/relengthening (±dL/dt). Intracellular Ca2+ was evaluated as Ca2+-induced Ca2+ release [difference in fura 2 fluorescent intensity (Delta FFI)] and fluorescence decay rate (tau ). Sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)2a, phospholamban (PLB), Na+-Ca2+ exchanger (NCX), GLUT4, and the serine-threonine kinase Akt were assessed by Western blot. RhoA and IGF-I/IGF-I receptor mRNA levels were determined by RT-PCR and Northern blot. OVE26 myocytes displayed decreased PS, ±dL/dt, and Delta FFI associated with prolonged TPS, TR90, and tau . SERCA2a, NCX, and Akt activation were reduced, whereas PLB and RhoA were enhanced in OVE26 hearts. GLUT4 was unchanged. IGF-I enhanced PS and Delta FFI in FVB but not OVE26 myocytes. IGF-I mRNA was increased, but IGF-I receptor mRNA was reduced in OVE26 hearts and livers. These results validate diabetic cardiomyopathy in OVE26 mice due to reduced SERCA2, NCX, IGF-I response, and Akt activation associated with enhanced RhoA level, suggesting a therapeutic potential for Akt and RhoA.

diabetic mouse; ventricular myocyte; excitation-contraction coupling; insulin-like growth factor I; sarco(endo)plasmic reticulum Ca2+-ATPase; sodium-calcium exchanger


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