Zbytek Blazej, Pfeffer Lawrence M, Slominski Andrzej T
Department of Histology and Immunology, Medical University of Gdansk, Gdansk, Poland.
J Invest Dermatol. 2003 Dec;121(6):1496-9. doi: 10.1111/j.1523-1747.2003.12612.x.
Treatment of human HaCaT keratinocytes with corticotropin-releasing hormone modulates cell proliferation and expression of inflammation markers. In this study we report that corticotropin-releasing hormone also inhibits nuclear factor-kappaB binding and transcriptional activity. Incubating cells in the absence of growth factors increased nuclear factor-kappaB activity; this effect was significantly attenuated by corticotropin-releasing hormone. Specifically, corticotropin-releasing hormone downregulated p50/p50 and p50/p65 dimers of nuclear factor-kappaB, diminished kappaB-driven CAT reporter gene activity and inhibited IkappaB-beta degradation. Moreover, corticotropin-releasing hormone inhibited the trans-cription of the nuclear factor-kappaB responsive genes, interleukin-2 and heat shock protein 90.
用促肾上腺皮质激素释放激素处理人HaCaT角质形成细胞可调节细胞增殖和炎症标志物的表达。在本研究中,我们报告促肾上腺皮质激素释放激素还可抑制核因子-κB的结合和转录活性。在无生长因子的情况下培养细胞可增加核因子-κB活性;促肾上腺皮质激素释放激素可显著减弱这种效应。具体而言,促肾上腺皮质激素释放激素下调核因子-κB的p50/p50和p50/p65二聚体,降低κB驱动的CAT报告基因活性,并抑制IκB-β降解。此外,促肾上腺皮质激素释放激素抑制核因子-κB反应性基因白细胞介素-2和热休克蛋白90的转录。