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首页> 外文期刊>The Journal of investigative dermatology. >Histamine Enhances the Production of Granulocyte-Macrophage Colony-Stimulating Factor via Protein Kinase Calpha and Extracellular Signal-Regulated Kinase in Human Keratinocytes.
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Histamine Enhances the Production of Granulocyte-Macrophage Colony-Stimulating Factor via Protein Kinase Calpha and Extracellular Signal-Regulated Kinase in Human Keratinocytes.

机译：组胺通过人角质形成细胞中的蛋白激酶Calpha和细胞外信号调节激酶增强粒细胞-巨噬细胞集落刺激因子的产生。

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摘要

The production of granulocyte-macrophage colony-stimulating factor (GM-CSF) in keratinocytes is related to the chronicity of atopic dermatitis. Mast cell-derived histamine contributes to the cross-talk between mast cells and keratinocytes. We examined the effects of histamine on GM-CSF production in human keratinocytes. Histamine increased GM-CSF secretion, mRNA stability and promoter activity. Activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) elements on the promoter were responsible for the activation by histamine. Histamine enhanced transcriptional activity and DNA binding of AP-1 and NF-kappaB. Histamine shifted AP-1 composition form c-Jun homodimers to c-Fos/c-Jun heterodimers, and transiently expressed c-Fos protein. Histamine rapidly induced the phosphorylation and degradation of inhibitory kappaB. Histamine induced membrane translocation of protein kinase Calpha. Histamine-induced GM-CSF production was completely abolished by H1 antagonist pyrilamine and conventional protein kinase C inhibitor Go6976, and partially suppressed by PD98059 which inhibits the activation of extracellular signal-regulated kinase. Go6976 and PD98059 suppressed histamine-induced c-Fos expression and AP-1 activation. Go6976 and PD98059 suppressed histamine-induced enhancement of NF-kappaB transcriptional activity. Histamine-induced phosphorylation and degradation of inhibitory kappaB was suppressed by Go6976, but not by PD98059. These results suggest that histamine may enhance GM-CSF production at transcriptional and posttranscriptional levels via H1 receptor, protein kinase Calpha and extracellular signal-regulated kinase.
机译：角质形成细胞中粒细胞巨噬细胞集落刺激因子（GM-CSF）的产生与特应性皮炎的慢性性有关。肥大细胞来源的组胺促进肥大细胞和角质形成细胞之间的串扰。我们检查了组胺对人角质形成细胞中GM-CSF产生的影响。组胺可增加GM-CSF分泌，mRNA稳定性和启动子活性。启动子上的激活蛋白-1（AP-1）和核因子-κB（NF-κB）元素负责组胺的激活。组胺增强AP-1和NF-κB的转录活性和DNA结合。组胺将AP-1组成从c-Jun同二聚体转变为c-Fos / c-Jun异二聚体，并瞬时表达c-Fos蛋白。组胺迅速诱导抑制性κB的磷酸化和降解。组胺诱导蛋白激酶Calpha的膜移位。组胺诱导的GM-CSF的产生被H1拮抗剂吡咯胺和常规的蛋白激酶C抑制剂Go6976完全消除，而被PD98059部分抑制，PD98059抑制了细胞外信号调节激酶的激活。 Go6976和PD98059抑制组胺诱导的c-Fos表达和AP-1激活。 Go6976和PD98059抑制了组胺诱导的NF-κB转录活性的增强。组胺诱导的磷酸化和抑制性kappaB的降解被Go6976抑制，但未被PD98059抑制。这些结果表明，组胺可以通过H1受体，蛋白激酶Calpha和细胞外信号调节激酶在转录和转录后水平上提高GM-CSF的产生。

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