巨噬细胞极化
炎症
促炎细胞因子
巨噬细胞
油红O
M2巨噬细胞
川地68
糖酵解
内分泌学
化学
缺铁
内科学
肿瘤坏死因子α
医学
癌症研究
生物
生物化学
新陈代谢
体外
免疫组织化学
贫血
脂肪生成
作者
Xiaorong Hu,Xinyong Cai,Ruisong Ma,Wenwen Fu,Changjiang Zhang,Xianjin Du
摘要
Abstract Atherosclerosis is still the major cause of morbidity and mortality all over the world. Recently, it has been reported increased levels of tissue iron increase the risk of atherosclerosis. However, the detailed mechanism of iron‐induced atherosclerosis progression is barely known. Here, we used apoE‐deficient mice models to investigate the effects of low iron diet (<0 mg iron carbonyl/kg), high iron diet (25,000 mg iron carbonyl/kg) on atherosclerosis in vivo. As exhibited, we observed that CD68 was significant enriched by high iron diet in apoE‐deficient mice. In addition, transforming growth factor β, tumor necrosis factor α, interleukin 6 (IL‐6), IL‐23, IL‐10, and IL‐1β levels were also greatly induced by high iron diet. Then, we found that the iron load promoted the inflammation response in macrophages. Moreover, macrophage polarization is a process by which macrophage can express various functional programs in activating macrophages. Here, we observed that iron‐load macrophages were polarized toward a proinflammatory macrophage phenotype. The polarization of M1 macrophage was promoted by ferric ammonium citrate (FAC) in bone marrow derived macrophages (BMDMs). Furthermore, ECAR and cellular OCR in BMDM with or without FAC was examined. As shown, BMDM indicated with 50 μM FAC showed a significant increase in basic state and maximal ECAR in contrast to the control group. However, there was no significant difference in OCR. This indicated that the glycolysis was involved in the polarization of M1 macrophage triggered by iron‐load. In conclusion, we indicated that the iron load exacerbates the progression of atherosclerosis via inducing inflammation and enhancing glycolysis in macrophages.
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