血清淀粉样蛋白A通过LOX-1促进系膜细胞摄取脂质

Serum Amyloid A Increases Lipid Uptake by Mesangial Cells via Lectin-like Oxidized Low-density Lipoprotein Receptor 1.

目的探讨SAA是否促进人肾小球系膜细胞(human mesangial cells,HMCs)摄取氧化低密度脂蛋白(oxidised low-density lipoprotein,Ox-LDL)及对其植物血凝素样受体1(lectin-like oxidised low-density lipoprotein receptor 1,LOX-1)表达的影响。方法应用油红“O”染色和流式细胞计数观察SAA对HMCs摄取脂质的影响,采用实时定量PCR和Western blot法测定SAA对LOX-1的表达。结果油红“O”染色和流式细胞计数显示SAA促进HMCs摄取Ox-LDL,流式细胞计数发现抗LOX-1抑制对Ox-LDL的摄取。SAA促进LOX-1 mRNA和蛋白的表达,提示SAA可能通过LOX-1介导对Ox-LDL摄取。结论SAA可通过LOX-1途径促进HMCs摄取脂质,针对SAA-LOX-1相关通路的治疗,可能是逆转肾小球硬化的潜在治疗靶点。

Objective To reveal whether serum amyloid A(SAA)increased oxidised low-density lipoprotein(Ox-LDL)uptake by human mesangial cells(HMCs)and its effect on expression of lectin-like Ox-LDL receptor 1(LOX-1).Methods Red oil“O”and flow cytometry were used to evaluate the effect of SAA on lipid uptake by HMCs.Effect of SAA on LOX-1 expression were calculated by real-time polymerase chain reaction(PCR)and western blotting.Results Red oil“O”and flow cytometry revealed that SAA promoted uptake of Ox-LDL by HMCs.Additinonally,increased uptake of Ox-LDL was inhibited by an anti-LOX-1 antibody through flow cytometry.Furthermore,SAA promoted LOX-1 mRNA and protein expression of HMCs,suggesting that enhanced uptake of Ox-LDL may be mediated by LOX-1 pathway.Conclusion SAA stimulates lipid uptake of HMC via LOX-1,therapy toward anti-SAA-LOX-1 pathway and related lipid disorders may be potential treatments for glomerulosclerosis.