ArticleActa physiologica Scandinavica2005
HSP20 phosphorylation and interstitial metabolites in hypoxia-induced dilation of swine coronary arteries.
Article in Acta physiologica Scandinavica, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- KV 7 channels are involved in hypoxia-induced vasodilatation of porcine coronary arteries.British journal of pharmacology · 2014Article
- Increase in periosteal angiogenesis through heat shock conditioning.Head & face medicine · 2011Article
- Phosphorylated HSP20 modulates the association of thin-filament binding proteins: caldesmon with tropomyosin in colonic smooth muscle.American journal of physiology. Gastrointestinal and liver physiology · 2010Article
- The small heat shock protein, HSPB6, in muscle function and disease.Cell stress & chaperones · 2010Review
- Adenosine concentration in the porcine coronary artery wall and A2A receptor involvement in hypoxia-induced vasodilatation.The Journal of physiology · 2006Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
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Abstract
objectiveHypoxia induces coronary artery dilation, but the responsible mechanism is largely unknown. Many stimuli induce arterial smooth muscle relaxation by reducing ser19-myosin regulatory light chain (MLC) phosphorylation. Other stimuli can induce smooth muscle relaxation without reductions in ser19-MLC phosphorylation. This form of relaxation has been termed force suppression and appears to be associated with heat shock protein 20 (HSP20) phosphorylation on ser16. We investigated whether hypoxia-induced sustained dilation in swine coronary arteries was promoted without ser19-MLC dephosphorylation and associated with ser16-HSP20 phosphorylation. Nitroglycerin vasodilation served as control.
methodsIn a pressure myograph, the tunica media of intact pre-contracted (PGF(2alpha); 10(-5) m) porcine coronary artery segments were cannulated using a microdialysis catheter. Diameter responses and interstitial lactate/pyruvate ratios were studied during 90 min hypoxia, hypoxia + reoxygenation (60 min), nitroglycerin (100 microm, 90 min), and nitroglycerin + wash-out (60 min). The arterial segments were snap-frozen and analysed for ser16-HSP20 phosphorylation and ser19-MLC phosphorylation.
resultsThe normalized diameter responses to hypoxia (6.1 +/- 4.3%) and nitroglycerin (12.6 +/- 1.6%) were both significantly greater than normoxic control arteries (-10.5 +/- 1.8%, anova, P < 0.05). Ser16-HSP20 phosphorylation was increased with hypoxia and nitroglycerin treatment and ser16-HSP20 phosphorylation correlated with changes in diameters (n = 29, r2 = 0.64, P < 0.001). Ser19-MLC phosphorylation was not significantly altered by hypoxia. The lactate/pyruvate ratio was significantly increased in hypoxic arteries but did not correlate with diameters or ser16-HSP20 phosphorylation.
conclusionSer16-HSP20 phosphorylation is a potential regulator of hypoxia-induced dilation in coronary arteries.
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