Heat induced HSP20 phosphorylation without increased cyclic nucleotide levels in swine carotid media.

Heat induced HSP20 phosphorylation without increased cyclic nucleotide levels in swine carotid media.
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DOI:
10.1186/1472-6793-3-3
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发表时间:
2003-04-25
期刊:
影响因子:
--
通讯作者:
Kaufman E
Kaufman E
中科院分区:
其他
文献类型:
--
作者:
Rembold CM;Kaufman E

文献摘要

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研究表明,猪颈动脉的热预处理可以增加ser16-热休克蛋白20 (HSP20)的磷酸化,并抑制力,即减少力,而ser19-肌球蛋白调节轻链(MRLC)的磷酸化仅有微小的降低。我们进一步研究了完整组胺刺激的猪颈动脉环的这种反应。在43°C和46°C之间存在热阈值,因此观察到ser16-HSP20磷酸化增加和力抑制。在44.5°C热处理后,增加的ser16-HSP20磷酸化持续16小时。在44.5°C下预处理猪颈动脉中膜增加了ser16-HSP20磷酸化,但没有增加[cAMP]或[cGMP],这提示了另一种机制,可能是磷酸酶抑制,导致ser16-HSP20磷酸化增加。47.5℃的热预处理通过降低MRLC磷酸化而不是通过大幅增加ser16-HSP20磷酸化来降低作用力。在假定的PKC位点的HSP20磷酸化没有随任何处理而改变。这些结果表明,多种机制可以诱导与ser16-HSP20磷酸化相关的力抑制:1)硝基血管扩张剂通过cGMP, 2)福斯克林通过cAMP, 2)热应激以环核苷酸独立的方式。
Heat pretreatment of swine carotid artery has been shown to increase ser16-heat shock protein 20 (HSP20) phosphorylation and suppress force, i.e., reduce force with only minimal reduction in ser19-myosin regulatory light chain (MRLC) phosphorylation. We further investigated this response in intact histamine stimulated swine carotid artery rings. There was a heat threshold such that increased ser16-HSP20 phosphorylation and force suppression were observed between 43°C and 46°C. The increased ser16-HSP20 phosphorylation persisted up to 16 hours after 44.5°C heat treatment. Pretreatment of swine carotid media at 44.5°C increased ser16-HSP20 phosphorylation without increases in [cAMP] or [cGMP], suggesting an alternate mechanism, perhaps phosphatase inhibition, for the increase in ser16-HSP20 phosphorylation. Heat pretreatment at 47.5°C reduced force by decreasing MRLC phosphorylation rather than by large increases in ser16-HSP20 phosphorylation. HSP20 phosphorylation at the putative PKC site did not change with any treatment. These results demonstrate that multiple mechanisms can induce force suppression that is correlated with ser16-HSP20 phosphorylation: 1) nitrovasodilators via cGMP, 2) forskolin via cAMP, and 2) thermal stress in a cyclic nucleotide independent manner.