Journal article
The Expression of GPIHBP1, an Endothelial Cell Binding Site for Lipoprotein Lipase and Chylomicrons, Is Induced by Peroxisome Proliferator-Activated Receptor-γ
Molecular endocrinology (Baltimore, Md.), Vol.22(11), pp.2496-2504
11/01/2008
DOI: 10.1210/me.2008-0146
PMCID: PMC2582544
PMID: 18787041
Abstract
Glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1), a protein in the lymphocyte antigen 6 (Ly-6) family, plays a key role in the lipolytic processing of triglyceride-rich lipoproteins. GPIHBP1 binds lipoprotein lipase and chylomicrons and is expressed along the luminal surface of microvascular endothelial cells. Lipolysis is known to be regulated by metabolic factors and is controlled at multiple levels, including the number of LPL binding sites on capillaries. Here, we tested the possibility that GPIHBP1 expression could be regulated by dietary perturbations and by peroxisome proliferator-activated receptors (PPARs). Gpihbp1 transcript levels in the heart and in brown and white adipose tissue increased with fasting and returned toward baseline after refeeding. A PPARγ agonist increased Gpihbp1 expression in adipose tissue, heart, and skeletal muscle, whereas PPARα and PPARδ agonists had no effect. Gpihbp1 was expressed in endothelial cells of embryoid bodies generated from mouse embryonic stem cells, and Gpihbp1 expression in embryoid bodies was up-regulated by a PPARγ agonist. Sequences upstream from exon 1 of Gpihbp1 contain a strong PPAR binding site, and that site exhibited activity in a luciferase reporter assay. Gpihbp1 transcript levels in brown and white adipose tissue were lower in endothelial cell PPARγ knockout mice than in littermate control mice, suggesting that PPARγ regulates Gpihbp1 expression in vivo. We conclude that GPIHBP1 is regulated by dietary factors and by PPARγ.
Details
- Title: Subtitle
- The Expression of GPIHBP1, an Endothelial Cell Binding Site for Lipoprotein Lipase and Chylomicrons, Is Induced by Peroxisome Proliferator-Activated Receptor-γ
- Creators
- Brandon S. J. Davies - University of Iowa, Fraternal Order of Eagles Diabetes Research CenterHironori Waki - Howard Hughes Medical InstituteAnne P. Beigneux - Supreme Council Of HealthEmily Farber - Supreme Council Of HealthMichael M. Weinstein - University of California, Los AngelesDamien C. Wilpitz - Howard Hughes Medical InstituteLi-Jung Tai - University of California, San DiegoRonald M. Evans - Salk Institute for Biological StudiesLoren G. Fong - Supreme Council Of HealthPeter Tontonoz - Howard Hughes Medical InstituteStephen G. Young - University of California, Los Angeles
- Resource Type
- Journal article
- Publication Details
- Molecular endocrinology (Baltimore, Md.), Vol.22(11), pp.2496-2504
- DOI
- 10.1210/me.2008-0146
- PMID
- 18787041
- PMCID
- PMC2582544
- ISSN
- 0888-8809
- eISSN
- 1944-9917
- Language
- English
- Date published
- 11/01/2008
- Academic Unit
- Fraternal Order of Eagles Diabetes Research Center; Biochemistry and Molecular Biology
- Record Identifier
- 9984024559802771
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