ATP结合盒转运子A1调控载脂蛋白M表达的通路

目的研究人肝癌细胞株HepG2中ATP结合盒转运子A1（ABCA1）是否通过肝受体同系物（LRH1）调节载脂蛋白M（apoM）的表达。方法分别用肝X受体激动剂GW3965或ABCA1阻滞剂DIDS作用于HepG2,应用RT-PCR法检测ABCA1、LRH1、apoM及apoAI的mRNA水平。结果与DMSO组比较,GW3965能显著增加ABCA1mRNA的表达（P〈0.01）,且呈剂量依赖性下调LRH1（P〈0.01）,但apoM和apoAI mRNA水平无明显变化（P〉0.05）;与GW3965单独作用组比较,GW3965与DIDS联合用药组apoM与apoAI的基因表达均明显下调（P〈0.05）,但ABCA1和LRH1水平均无明显变化（P〉0.05）。结论 ABCA1不通过LRH1调节apoM的表达。

Role of ABCAl on Regulation of apoM Expression Pathway

Objective To investigate whether ATP-binding cassette transporter A1（ABCA1） regulating apolipoprotein M expression being mediated via the liver receptor homolog-1（LRHl） pathway in HepG2 cellls.Methods HepG2 cells were incubated in presence of liver X receptor（LXR） agonists GW3965 with or without ABCAl antagonist disodium 4,4＇-diisothiocyanatostilbene-2,2＇-disulfonate （DIDS）.The mRNA levels of ABCAl,LRHl,apoM and apoAI were determined by the real-time RT-PCR. Results GW3965 was able to significantly up-regulate ABCAl（P〈0.01） and down-regulate LRHl expression（P〈0.01）,however,neither apoM nor apoAI expression was significantly affected（P 0.05）.Combination of GW3965 and DIDS had effects on the inhibition of apoM or apoAI expression in HepG2 cells（P〈0.05）,however,ABCAl or LRHl mRNA expression had no significance statistically （P〈0.05）.Conclusion The present study demonstrates that ABCAl mediated apoM expression does not via the LRHl pathway.