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Articles in PresS, published online ahead of print January 2, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00307.2001
Submitted on July 5, 2001
Accepted on December 31, 2001
1 Biology, Marquette University, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: sherwood{at}physiology.med.uvm.edu.
In smooth muscle cells (SMCs) isolated from rabbit carotid, femoral and saphenous arteries, relative myosin isoform mRNA levels were measured in reverse transcriptase-polymerase chain reactions (RT-PCRs) to test for correlations between myosin isoform expression and unloaded shortening velocity. Unloaded shortening velocity and %SM2 and %MLC17b mRNA levels were not significantly different in single SMCs isolated from the luminal and adluminal regions of the carotid media. Saphenous artery SMCs shortened significantly faster (p < 0.05) than femoral SMCs, had more SM2 mRNA (p<0.05) than carotid SMCs, less MLC17b mRNA (p<0.001) and higher tissue levels of SMB mRNA (p<0.05) than carotid and femoral SMCs. No correlations were found between %SM2 and %MLC17b mRNA levels and unloaded shortening velocity in SMCs from these arteries. We have previously shown that MHC SM1/SM2, SMA/SMB and MLC17 a/b isoform mRNA levels correlate with protein expression for these isoforms in rabbit SM tissues. Thus, we interpret these results to suggest that: 1) SMC myosin isoform expression and unloaded shortening velocity do not vary with distance from the lumen of the carotid artery but do vary in arteries located longitudinally within the arterial tree, 2) MHC SM1/SM2 and/or MLC17 a/b isoform expression does not correlate with unloaded shortening velocity and 3) that intracellular expression of the MHC SM1/SM2 and MLC17 a/b isoforms is not co-regulated.
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