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Role of Apolipoprotein E Receptors in Regulating the Differential in vivo Neurotrophic Effects of Apolipoprotein E
Abstract
Apolipoprotein E (apoE) is known to bind to at least five receptors, including the low-density lipoprotein (LDL) receptor-related protein (LRP), very low density LDL receptor (VLDL-R), LDL-R, apoE receptor 2 (apoER2), and megalin/gp330. In this context, the main objective of the present study was to better understand the contributions of LRP and LDL-R to the in vivo neurotrophic effects of apoE. For this purpose, apoE-deficient and receptor-associated protein (RAP)-deficient mice were infused with recombinant apoE3, RAP, or saline. Infusion of apoE3 into apoE-deficient mice resulted in amelioration of degenerative alterations of pyramidal neurons, but had no effect on somatostatin-producing interneurons. In contrast, infusion of apoE3 into RAP-deficient mice resulted in amelioration of degenerative alterations of somatostatin-producing interneurons. LRP and LDL-R levels were significantly reduced in RAP-deficient mice, but significantly increased in the apoE-deficient mice. In contrast, levels of apoE were reduced in the RAP-deficient mice compared to wildtype controls, suggesting that neurotrophic effects of apoE3 in the RAP-deficient mice were related to a combined deficit in endogenous apoE and selected apoE receptors. Furthermore, in apoE-deficient mice, infusion of apoE3 had a neurotrophic effect on somatostatin-producing interneurons only when combined with RAP, suggesting that increased expression of apoE receptors in apoE-deficient mice prevented apoE from rescuing so…
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RAP-/- mice were selected because previous studies have shown that it is possible to reduce the levels of LRP and other lipoprotein receptors by deleting the RAP gene.
“RAPϪ/Ϫ mice were selected because previous studies have shown that it is possible to reduce the levels of LRP and other lipoprotein receptors (Van Uden et al., 1999a;Veinbergs et al., 2001) by deleting the R AP gene”
From Increased Extracellular Amyloid Deposition and Neurodegeneration in Human Amyloid Precursor Protein Transgenic Mice Deficient in Receptor-Associated Protein (2002) · cites this paper as Veinbergs et al., 2001
RAP−/− mice display deficient somatostatin release and memory deficits in the water maze that are ameliorated by apoE.
“Furthermore, RAPϪ/Ϫ mice display deficient somatostatin release and memory deficits in the water maze (Van Uden et al., 1999a) that are ameliorated by another LRP ligand, namely apoE (Veinbergs et al., 2001).”
From Increased Extracellular Amyloid Deposition and Neurodegeneration in Human Amyloid Precursor Protein Transgenic Mice Deficient in Receptor-Associated Protein (2002) · cites this paper as Veinbergs et al., 2001
In the RAP-/- mice, LRP levels are reduced by 75-80%, whereas levels of LDL-R and VLDL-R are reduced by 40-50%.
“However, it is worth noting that, in the RAPϪ/Ϫ mice, LRP levels are reduced by 75-80%, whereas levels of LDL-R and VLDL-R are reduced by 40 -50% (Veinbergs et al., 2001).”
From Increased Extracellular Amyloid Deposition and Neurodegeneration in Human Amyloid Precursor Protein Transgenic Mice Deficient in Receptor-Associated Protein (2002) · cites this paper as Veinbergs et al., 2001
RAP regulates other members of the LRP family, such as LRP1B, SorLA/LR11, LDL-R and VLDL-R.
“RAP also regulates other members of the LRP family, such as LRP1B [17], SorLA/LR11[45], LDL-R and VLDL-R [46]”
From Receptor-Associated Protein (RAP) Plays a Central Role in Modulating Aβ Deposition in APP/PS1 Transgenic Mice (2008) · cites this paper as [46]
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Metadata
- Authors
- Veinbergs, I., Van Uden, E., Mallory, M., Alford, M., McGiffert, C., DeTeresa, R., Orlando, R., & Masliah, E.
- Venue
- Experimental Neurology
- Publisher
- Elsevier BV
- Published
- 2001-07
- Volume
- 170
- Issue
- 1
- Pages
- 15-26
- ISSN
- 0014-4886
- Cited by
- 29
- References
- 3
- Language
- en
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