Variable expression of SM1 and SM2 SM-MHC tail isoforms primarily affects the final length of smooth muscle cells rather than their shortening velocity.
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May influence smooth muscle cell length but not velocity in animals; hypothesis-generating for human vascular mechanics.
The functional significance of the variable expression of the smooth muscle myosin heavy chain (SM-MHC) tail isoforms, SM1 and SM2, was examined at the mRNA level (which correlates with the protein level) in individual permeabilized rabbit arterial smooth muscle cells (SMCs). The length of untethered single permeabilized SMCs was monitored during unloaded shortening in response to increased Ca 2+ (pCa 6.0), histamine (1 μM), and phenylephrine (1 μM). Subsequent to contraction, the relative expression of SM1 and SM2 mRNAs from the same individual SMCs was determined by reverse transcription-polymerase chain reaction amplification and densitometric analysis. Correlational analyses between the SM2-to-SM1 ratio and unloaded shortening in saponin- and α-toxin-permeabilized SMCs ( n = 28) reveal no significant relationship between the SM-MHC tail isoform ratio and unloaded shortening velocity. The best correlations between SM2/SM1 and the contraction characteristics of untethered vascular SMCs were with the minimum length attained following contraction ( n = 20 and r = 0.72 for α-toxin, n = 8 and r = 0.78 for saponin). These results suggest that the primary effect of variable expression of the SM1 and SM2 SM-MHC tail isoforms is on the cell final length and not on shortening velocity.
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Meer et al. (1997) studied this question.
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