Reduced VLDL clearance in Apoe(-/-)Npc1(-/-) mice is associated with increased Pcsk9 and Idol expression and decreased hepatic LDL-receptor levels

J Lipid Res. 2010 Sep;51(9):2655-63. doi: 10.1194/jlr.M006163. Epub 2010 Jun 18.

Abstract

Niemann-Pick type C1 (NPC1) promotes the transport of LDL receptor (LDL-R)-derived cholesterol from late endosomes/lysosomes to other cellular compartments. NPC1-deficient cells showed impaired regulation of liver_X receptor (LXR) and sterol regulatory element-binding protein (SREBP) target genes. We observed that Apoe(-/-)Npc1(-/-) mice displayed a marked increase in total plasma cholesterol mainly due to increased VLDL, reflecting decreased clearance. Although nuclear SREBP-2 and Ldlr mRNA levels were increased in Apoe(-/-)Npc1(-/-) liver, LDL-R protein levels were decreased in association with marked induction of proprotein convertase subtilisin/kexin type 9 (Pcsk9) and inducible degrader of the LDL-R (Idol), both known to promote proteolytic degradation of LDL-R. While Pcsk9 is known to be an SREBP-2 target, marked upregulation of IDOL in Apoe(-/-)Npc1(-/-) liver was unexpected. However, several other LXR target genes also increased in Apoe(-/-)Npc1(-/-) liver, suggesting increased synthesis of endogenous LXR ligands secondary to activation of sterol biosynthesis. In conclusion, we demonstrate that NPC1 deficiency has a major impact on VLDL metabolism in Apoe(-/-) mice through modulation of hepatic LDL-R protein levels. In contrast to modest induction of hepatic IDOL with synthetic LXR ligands, a striking upregulation of IDOL in Apoe(-/-)Npc1(-/-) mice could indicate a role of endogenous LXR ligands in regulation of hepatic IDOL.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apolipoproteins E* / genetics
  • Apolipoproteins E* / metabolism
  • Cells, Cultured
  • Cholesterol / blood
  • Cholesterol, VLDL / metabolism*
  • Intracellular Signaling Peptides and Proteins
  • Lamin Type A / metabolism
  • Liver / physiology*
  • Liver X Receptors
  • Macrophages, Peritoneal / cytology
  • Macrophages, Peritoneal / metabolism
  • Mice
  • Mice, Knockout
  • Niemann-Pick C1 Protein
  • Orphan Nuclear Receptors / genetics
  • Orphan Nuclear Receptors / metabolism
  • Proprotein Convertase 9
  • Proprotein Convertases
  • Proteins* / genetics
  • Proteins* / metabolism
  • Receptors, LDL / metabolism*
  • Serine Endopeptidases / genetics
  • Serine Endopeptidases / metabolism*
  • Sterol Regulatory Element Binding Protein 1 / genetics
  • Sterol Regulatory Element Binding Protein 1 / metabolism
  • Sterol Regulatory Element Binding Protein 2 / genetics
  • Sterol Regulatory Element Binding Protein 2 / metabolism
  • Triglycerides / blood
  • Ubiquitin-Protein Ligases / genetics
  • Ubiquitin-Protein Ligases / metabolism*

Substances

  • Apolipoproteins E
  • Cholesterol, VLDL
  • Intracellular Signaling Peptides and Proteins
  • Lamin Type A
  • Liver X Receptors
  • Niemann-Pick C1 Protein
  • Npc1 protein, mouse
  • Orphan Nuclear Receptors
  • Proteins
  • Receptors, LDL
  • Sterol Regulatory Element Binding Protein 1
  • Sterol Regulatory Element Binding Protein 2
  • Triglycerides
  • Cholesterol
  • Mylip protein, mouse
  • Ubiquitin-Protein Ligases
  • Pcsk9 protein, mouse
  • Proprotein Convertase 9
  • Proprotein Convertases
  • Serine Endopeptidases