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KLF4 regulates the expression of interleukin-10 in RAW264.7 macrophages.

机译:KLF4调节RAW264.7巨噬细胞中白介素10的表达。

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摘要

Kruppel-like factor 4 (KLF4) is an evolutionarily conserved zinc finger-containing transcription factor. In the current study, RAW264.7 murine macrophages were treated with Escherichia coli lipopolysaccharide (LPS) to determine the expression of KLF4. A full-length cDNA or antisense oligonucleotides of KLF4 was transfected into RAW264.7 macrophages, and the expression and release of IL-10 were analyzed by RT-PCR and ELISA. The transcription and DNA binding activities of KLF4 to the IL-10 promoter were detected by the luciferase reporter and electrophoretic mobility shift assays. The results showed that treatment of RAW264.7 macrophages with LPS resulted in a dose- and time-dependent increase in KLF4 protein levels; KLF4 overexpression increased the expression of IL-10, while KLF4 inhibition decreased the expression of IL-10. The overexpression of KLF4 promoted the transcription and DNA binding activities of KLF4 to the IL-10 promoter. These results indicate that KLF4 plays an important role in regulating the expression of IL-10.
机译:Kruppel样因子4(KLF4)是进化上保守的含锌指的转录因子。在当前的研究中,RAW264.7鼠巨噬细胞用大肠杆菌脂多糖(LPS)处理以确定KLF4的表达。将KLF4的全长cDNA或反义寡核苷酸转染到RAW264.7巨噬细胞中,并通过RT-PCR和ELISA分析IL-10的表达和释放。通过荧光素酶报道分子和电泳迁移率变动分析来检测KLF4对IL-10启动子的转录和DNA结合活性。结果表明,用LPS处理RAW264.7巨噬细胞会导致KLF4蛋白水平呈剂量和时间依赖性增加; KLF4过表达增加了IL-10的表达,而KLF4抑制则降低了IL-10的表达。 KLF4的过表达促进了KLF4对IL-10启动子的转录和DNA结合活性。这些结果表明KLF4在调节IL-10的表达中起重要作用。

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