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Department of Physiology and Biophysics, University of California, Irvine, California
Submitted 20 October 2005 ; accepted in final form 9 January 2006
Hypertension has been shown to cause cardiac hypertrophy and a shift in myosin heavy chain (MHC) gene expression from the faster 
- to slower 
-MHC isoform. The expression of the - and -MHC pre-mRNAs, mRNAs, as well as the newly discovered antisense -RNA were analyzed in three regions of the normal control (NC) and 12-day pressure-overloaded (AbCon) hearts: the left ventricle apex, left ventricle base, and the septum. The RNA analyses in the AbCon heart targeted both the 5' and the 3' ends of each RNA molecule. -MHC mRNA expression significantly increased relative to control in all three regions, regardless of the target site (5' or 3' end). In contrast, -MHC pre-mRNA expression in the AbCon heart depended on the site of the measurement (5' vs. 3' end). For example, whereas the pre-mRNA did not change when targeted at the 3' end (last intron), it increased significantly in the AbCon heart when measurement targeted the 5' end (2nd intron) of the 25-kb molecule. Analyses of the antisense -RNA revealed that its expression in the AbCon heart was significantly decreased relative to control regardless of its measurement site. A negative correlation was observed between the -mRNA expression and the antisense -RNA (P < 0.05), suggesting an inhibitory role of antisense RNA on the sense -MHC gene expression. In contrast, a positive correlation was observed between the antisense -RNA and the -MHC pre-mRNA (P < 0.05). This latter observation along with the -MHC gene position relative to that of the -antisense suggest that the -MHC sense and -antisense transcription are coregulated likely via common intergenic regulatory sequences. Our results suggest that the increased -MHC expression in the AbCon heart not only is the result of increased -MHC transcription but also involves an antisense -RNA regulation scheme. Although the exact mechanism concerning antisense regulation is not clear, it could involve modulation of both transcriptional activity of the -MHC gene and posttranscriptional processing.
premRNA; gene transcription; posttranscription; hypertension; RT-PCR; Sprague-Dawley rats
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