白细胞介素-27 通过 JAK2/STAT3 通路促进巨噬细胞 ABCA1 表达抑制泡沫细胞形成。
Interleukin-27 inhibits foam cell formation by promoting macrophage ABCA1 expression through JAK2/STAT3 pathway.
机构信息
Department of ICU, First Affiliated Hospital of University of South China, Hengyang 421001, Hunan, China.
Institute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, China.
出版信息
Biochem Biophys Res Commun. 2014 Oct 3;452(4):881-7. doi: 10.1016/j.bbrc.2014.08.120. Epub 2014 Sep 4.
The purpose of this study is to determine whether IL-27 regulates macrophage ABCA1 expression, foam cell formation, and also explore the underlying mechanisms. Here, we revealed that IL-27 decreased lipid accumulation in THP-1 derived macrophages through markedly enhancing cholesterol efflux and increasing ABCA1 expression at both protein and mRNA levels. Our study further demonstrated that IL-27 increased ABCA1 level via activation of signal transducer and activator of transcription 3 (STAT3). Inhibition of Janus kinase 2, (JAK2)/STAT3 suppressed the stimulatory effects of IL-27 on ABCA1 expression. The present study concluded that IL-27 reduces lipid accumulation of foam cell by upregulating ABCA1 expression via JAK2/STAT3. Therefore, targeting IL-27 may offer a promising strategy to treat atherosclerotic vascular disease.
本研究旨在确定 IL-27 是否调节巨噬细胞 ABCA1 的表达，以及泡沫细胞的形成，并探讨其潜在的机制。在这里，我们揭示了 IL-27 通过显著增强胆固醇流出和增加 ABCA1 蛋白和 mRNA 水平来减少 THP-1 衍生巨噬细胞中的脂质积累。我们的研究进一步表明，IL-27 通过激活信号转导和转录激活因子 3（STAT3）来增加 ABCA1 水平。抑制 Janus 激酶 2（JAK2）/STAT3 抑制了 IL-27 对 ABCA1 表达的刺激作用。本研究得出结论，IL-27 通过 JAK2/STAT3 上调 ABCA1 表达来减少泡沫细胞的脂质积累。因此，靶向 IL-27 可能为治疗动脉粥样硬化性血管疾病提供一种有前途的策略。
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