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Brian N. Finck, John J. Lehman, Teresa C. Leone, Michael J. Welch, Michael J. Bennett, Attila Kovacs, Xianlin Han, Richard W. Gross, Ray Kozak, Gary D. Lopaschuk, Daniel P. Kelly
Published in Volume 109, Issue 1
J Clin Invest. 2002; 109(1):121–130 doi:10.1172/JCI14080
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Figure 1

Increased expression of PPARα target genes in diabetic mouse myocardium. (a) Bars represent mean (± SEM) mRNA levels as determined by phosphorimager analysis of Northern blots performed with RNA isolated from mouse ventricle, shown as arbitrary units (AU) corrected for GAPDH signal intensity and normalized to the value of vehicle-injected controls (= 1.0). *P < 0.05 versus vehicle-injected mice (n = 4 for each group). A representative autoradiograph of the Northern blot studies is shown at the right. Each lane contained 15 μg total RNA isolated from mice 6 weeks after an injection of saline (vehicle) or a single dose of STZ (180 mg/kg). The blot was sequentially hybridized with the radiolabeled cDNA probes shown on the left. (b) Increased expression of PPARα target genes in db/db diabetic mice. Bars represent mRNA levels shown as arbitrary units (AU) corrected for GAPDH signal intensity and normalized to the value of db/+ littermate controls (= 1.0). *P < 0.05 versus db/+ littermate controls; n = 5 for each group. A representative autoradiograph is shown at the right. Each lane contained 15 μg of ventricular total RNA isolated from 10-week-old heterozygote control (db/+) or littermate diabetic (db/db) mice.