Heat Shock Inhibits Cytokine-Induced Nitric Oxide Synthase Expression by Rat and Human Islets* * This work was supported by research grants from the NIH (DK-52194) and The Tobacco Research Council.

Heat Shock Inhibits Cytokine-Induced Nitric Oxide Synthase Expression by Rat and Human Islets* * This work was supported by research grants from the NIH (DK-52194) and The Tobacco Research Council.
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热休克抑制大鼠和人类胰岛细胞因子诱导的一氧化氮合酶表达* * 这项工作得到了 NIH (DK-52194) 和烟草研究委员会研究经费的支持。

DOI:
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发表时间:
1998
期刊:
影响因子:
4.8
通讯作者:
J. A. Corbett
J. A. Corbett
中科院分区:
医学2区
文献类型:
--
作者:
A. Scarim;M. Heitmeier;J. A. Corbett

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In this study the effects of heat shock on interleukin-1β (IL-1)-induced inhibition of islet metabolic function were examined. Treatment of rat islets for 18 h with IL-1 results in a potent inhibition of glucose-stimulated insulin secretion. The inhibitory effects of IL-1 on insulin secretion are completely prevented if islets are pretreated for 60 min at 42 C before cytokine stimulation. Heat shock also prevents IL-1-induced inhibition of insulinoma RINm5F cell mitochondrial aconitase activity. The protective effects of heat shock on islet metabolic function are associated with the inhibition of IL-1-stimulated inducible nitric oxide synthase (iNOS or NOS II) expression. Islets heat shocked for 60 min at 42 C fail to express iNOS (messenger RNA or protein) or produce nitrite in response to IL-1. IL-1-induced iNOS expression by rat islets requires activation of the transcriptional regulator nuclear factor κB (NF-κB). Heat shock prevents IL-1- induced NF-κB nuclear localization by inhibiting inhibitory pro...
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