TO901317Regulating Apolipoprotein M Expression Mediates Via The Farnesoid X Receptor Pathway In Caco-2Cells

[Objective]: Apolipoprotein M (ApoM) may have potentialantiatherosclerotic properties. It has been approved that ApoM expressioncould be regulated by many introcellar and extrocellar factors. In this studywe investigated mechanism of ApoM expression in Caco-2cells stimulatedby the liver X receptor (LXR) agonist TO901317(TO).[Methods]: Caco-2cells were cultured in the presence of either LXRagonist TO901317, farnesoid X receptor (FXR) antagonist guggulsterone (Gu)or Gu together with TO901317at different concentrations. The mRNA levelsof ApoM, short heterodimer partner1(SHP1), liver receptor homologue-1(LRH-1) and ATP-binding cassette transporter A1(ABCA1) were determinedby the real-time RT-PCR.[Results]: Coca-2cell cultured with TO901317alone significantlyincreased the mRNA levels of ApoM, SHP1and LRH-1(p<0.05), whereasguggulsterone alone strongly inhibited the mRNA levels of ApoM, SHP1andLRH-1(p<0.05). Moreover, guggulsterone could abolish the TO901317enhanced mRNA levels of ApoM, SHP1and LRH-1(p<0.05). [Conclusion]: The present study clearly demonstrated that LXR-agonistTO901317induced ApoM expression in Caco-2cells is mediated via theLXR/FXR pathway.