Abstract
BackgroundApolipoprotein M (apoM) may have potential antiatherosclerotic properties. It has been reported that apoM expression could be regulated by many intracellar and extracellar factors. In the present study we further investigated regulation of apoM expression in Caco-2 cells stimulated by a liver X receptor (LXR) agonist, TO901317.Materials and methodsCaco-2 cells were cultured in the presence of either TO901317, farnesoid X receptor (FXR) antagonist guggulsterone or TO901317 together with guggulsterone at different concentrations for 24 hrs. The mRNA levels of ATP-binding cassette transporter A1 (ABCA1), apoA1, apoM, liver receptor homologue-1 (LRH-1) and short heterodimer partner 1 (SHP1) were determined by real-time RT-PCR.ResultsWhen Caco-2 cell cultured with TO901317 alone, the mRNA levels of ABCA1, apoA1, apoM, LRH-1 and SHP1 were significantly increased with dose-dependent manners (p < 0.05), whereas when the cells cultured with guggulsterone alone, the mRNA levels of apoM, SHP1 and LRH-1 (p < 0.05) were strongly inhibited. Moreover, guggulsterone could abolish the TO901317 enhanced mRNA levels of apoA1 apoM, SHP1 and LRH-1.ConclusionThe present study demonstrated that LXR agonist TO901317 induced apoM expression in Caco-2 cells might be mediated via the LXR/FXR pathway.
Highlights
With the aging population and changing lifestyles, the incidence of cardiovascular diseases (CVD) has gradually increased [1]
When Caco-2 cell cultured with TO901317 alone, the mRNA levels of ATP-binding cassette transporter A1 (ABCA1), apoA1, Apolipoprotein M (apoM), liver receptor homologue-1 (LRH-1) and short heterodimer partner 1 (SHP1) were significantly increased with dose-dependent manners (p < 0.05), whereas when the cells cultured with guggulsterone alone, the mRNA levels of apoM, SHP1 and LRH-1 (p < 0.05) were strongly inhibited
The present study demonstrated that liver X receptor (LXR) agonist TO901317 induced apoM expression in Caco-2 cells might be mediated via the LXR/farnesoid X receptor (FXR) pathway
Summary
With the aging population and changing lifestyles, the incidence of cardiovascular diseases (CVD) has gradually increased [1]. Studies have demonstrated that serum concentrations of apolipoprotein (apo) AI and apoB have significantly correlation with the occurrences of CVD [3,4], and other apolipoproteins may involve in the initiation and progression of the diseases [5]. Recent investigations have suggested that apoM may participate in the HDL-related biological activities as an important component of HDL particle on the protection of endothelial cells [8]. It has been reported that apoM expression could be regulated by many intracellar and extracellar factors. In the present study we further investigated regulation of apoM expression in Caco-2 cells stimulated by a liver X receptor (LXR) agonist, TO901317
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