کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5505114 1400261 2017 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
LIGHT is increased in patients with coronary disease and regulates inflammatory response and lipid metabolism in oxLDL-induced THP-1 macrophages
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
LIGHT is increased in patients with coronary disease and regulates inflammatory response and lipid metabolism in oxLDL-induced THP-1 macrophages
چکیده انگلیسی
Inflammation is critical for the progression of hyperlipidemia. Although the exact mechanism through which inflammation affects hyperlipidemia is not very clear, evidence suggests that the tumor necrosis factor superfamily member 14 (TNFSF14/LIGHT)LIGHT might regulate lipid metabolism. In this study we investigated the expression of LIGHT in patients with different stages of coronary disease. The expression of lipid metabolism-related enzymes and inflammation-related proteins were further explored in oxidized low-density lipoproteins (oxLDL)-induced THP-1 macrophages. We found that LIGHT is highly expressed and companied with severe inflammations in patients with coronary disease. LIGHT significantly enhanced inflammation response in oxLDL-induced THP-1 macrophages. We further demonstrated that LIGHT markedly decreased the levels of lipolytic genes and increased the expressions of lipogenic genes in oxLDL-induced THP-1 macrophages. In addition, our results showed that LIGHT exerts its pro-inflammatory and pro-lipogenesis roles through activating nuclear factor-kappa B (NF-κB) signaling pathway. Taken together our study has demonstrated that LIGHT NF-κB-dependently exacerbates inflammation response and promotes lipid accumulation, and provided a new potential target for treatment of hyperlipidemia-related disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 490, Issue 3, 26 August 2017, Pages 732-738
نویسندگان
, , , ,