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Am J Physiol Cell Physiol (October 27, 2004). doi:10.1152/ajpcell.00269.2004
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Submitted on June 7, 2004
Accepted on October 21, 2004

Heat shock protein 20 mediated force suppression in forskolin relaxed swine carotid artery

Melissa K Meeks1, Marcia L Ripley1, Zhicheng Jin1, and Christopher M Rembold1*

1 Internal Medicine, University of Virginia, Charlottesville, VA, USA

* To whom correspondence should be addressed. E-mail: crembold{at}virginia.edu.

Increases in cyclic nucleotide levels induce smooth muscle relaxation by deactivation (reductions in MRLC phosphorylation, e.g. by reduced [Ca2+]) or by force suppression (reduction in force without reduction in MRLC phosphorylation). Ser16-HSP20 phosphorylation is the proposed mediator of force suppression. Our goal was to evaluate three potential hypotheses whereby ser16-HSP20 phosphorylation could regulate smooth muscle force: 1) a threshold level of HSP20 phosphorylation could inactivate a thin filament as a whole, 2) phosphorylation of a single HSP20 could fully inactivate a small region of a thin filament, or 3) HSP20 phosphorylation could weakly inhibit myosin binding either at the thin or thick filament level. We tested these hypotheses by analyzing the dependence of force on ser16-HSP20 phosphorylation in swine carotid media. First, we determined that swine HSP20 has a second phosphorylation site at ser157. Ser157-HSP20 phosphorylation values were high and did not change during contractile activation or forskolin-induced relaxation. Forskolin significantly increased ser16-HSP20 phosphorylation. The relation between ser16-HSP20 phosphorylation and force remained linear and was shifted downward in partially activated muscles that were relaxed with forskolin. Neither forskolin nor nitroglycerin induced actin depolymerization as detected by the F/G actin ratio method in smooth muscle homogenates. Both of these results suggest that force suppression does not occur by the first hypothesis (inactivation of a thin filament as a whole). Our data is more consistent with the second or third hypothesis that force suppression is mediated by full or partial inhibition of local myosin binding at the thin or thick filament level.




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