A liver X receptor (LXR)-beta alternative splicing variant (LXRBSV) is preferentially expressed in the pituitary

Biochem Biophys Res Commun. 2010 Apr 9;394(3):548-52. doi: 10.1016/j.bbrc.2010.03.013. Epub 2010 Mar 6.

Abstract

We have recently reported that an alternative splicing variant of liver X receptor (LXR)-beta acts as an RNA co-activator, which is referred to as LXRBSV. The in vivo role of LXRBSV is yet to be clarified. The LXRBSV gene is expressed in various tissues including the liver and brain. We evaluated the gene expression of LXRBSV in various regions of the brain using real-time quantitative PCR assays in the current study and found that LXRBSV is abundantly expressed in the pituitary. 5'-rapid amplification of cDNA ends (5'-RACE) revealed that the transcriptional start site (TSS) of LXRBSV is located 40 base pairs (bp) downstream of LXR-beta. We prepared two promoter constructs: -1598/+35 bp and -1598/+75 bp in pGL4 for LXR-beta and LXRBSV, respectively. The latter promoter construct demonstrated significantly higher activity than the former construct in GH3 cells derived from the rat pituitary. On the contrary, the promoter activities of these two constructs were indistinguishable in Hepa1-6 cells derived from mouse hepatocytes. Furthermore, the promoter region specific for LXRBSV itself exerted promoter activity in GH3 cells but not in Hepa1-6 cells. Taken together, we have concluded that LXRBSV is preferentially transcribed and expressed in the pituitary, indicating that LXRBSV plays a role in regulating pituitary gene expression. These data provide clues to elucidating the physiological relevance of LXRBSV.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alternative Splicing*
  • Animals
  • Cell Line
  • Gene Expression
  • Hepatocytes / metabolism
  • Humans
  • Liver X Receptors
  • Mice
  • Orphan Nuclear Receptors / genetics*
  • Pituitary Gland / metabolism*
  • Promoter Regions, Genetic
  • Rats
  • Transcription Initiation Site
  • Transcriptional Activation*

Substances

  • Liver X Receptors
  • Orphan Nuclear Receptors