Resistin up-regulates LPL expression through the PPARγ-dependent PI3K/AKT signaling pathway impacting lipid accumulation in RAW264.7 macrophages. (July 2019)

• Record Type: Journal Article
• Authors: Li, Bi; Fang, Jing; He, Tingting; Yin, Sirui; Yang, Mingxian; Cui, Hengmin; Ma, Xiaoping; Deng, Junliang; Ren, Zhihua; Hu, Yanchun; Ye, Gang; Zhang, Ming; Geng, Yi; Gou, Liping; Zuo, Zhicai
• Is Part Of: Cytokine. Volume 119(2019)
• Page Start: 168
• Page End: 174
• Publication Date: 2019-07
• Subjects: Resistin -- Macrophages -- Lipoprotein lipase -- Phosphatidylinositol 3-kinase -- Serine-threonine protein kinase -- Peroxisome proliferator-activated receptor; Cytokines -- Periodicals; 571.844
• DOI: 10.1016/j.cyto.2019.03.016
• Languages: English
• ISSNs: 1043-4666

Abstract

Highlights: The lipid accumulation in resistin-stimulated macrophages was correlated with LPL. Resistin up-regulated LPL to accelerate lipid accumulation via PPARγ/PI3K/AKT. This study might provide targets for the prevention of lipid metabolic disorders. Abstract: Resistin is a cysteine-rich cytokine, which has been indicated as a mediator of insulin resistance and inflammation. Previous studies demonstrated that lipoprotein lipase (LPL) was an important enzyme that could mediate lipid accumulation in macrophages. Additionally, the intracellular molecules phosphatidylinositol 3-kinase (PI3K)/serine-threonine protein kinase (AKT)/peroxisome proliferator-activated receptor (PPARγ) were supposed to be involved in the lipid accumulation process in cells. However, it remains unclear whether resistin was correlated with the dysregulation of lipid metabolism in macrophages. The present study investigated that resistin could up-regulate the expression of LPL and increase the contents of intracellular triglyceride (TG) and total cholesterol (TC) in RAW264.7 macrophages. In addition, intracellular molecules PI3K, AKT and PPARγ were significantly up-regulated and activated in resitin-stimulated RAW264.7 macrophages ( P < 0.05 ). In contrast, the effects of resistin on RAW264.7 macrophages could be abrogated by specific inhibitors for LPL (LPL-siRNA) and PI3K/AKT signaling pathway (LY294002). All together, this study demonstrated that resistin could up-regulate the expression of LPL and induce lipid accumulation in RAW264.7 macrophages. More importantly, the PPARγ-dependent PI3K/AKT signaling pathway was relevant to the lipid accumulation process in resistin-stimulated macrophages.