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Hypercholesterolemia in low density lipoprotein receptor knockout mice and its reversal by adenovirus-mediated gene delivery.
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Total plasma cholesterol was not affected (80.1 ± 10.1 mg/dl versus 81.4 ± 9.1; n = 20; P = 0.68).
“Total plasma cholesterol was not affected (80.1 ± 10.1 mg/dl versus 81.4 ± 9.1; n = 20; P = 0.68) (Figure 2B), which contrasts the phenotype of LDLR and LRP mutant mice (15,49).”
From Liver heparan sulfate proteoglycans mediate clearance of triglyceride-rich lipoproteins independently of LDL receptor family members (2007) · cites this paper as [49]
LDLR deficiency leads to a large increase in levels of apoB-100-bearing cholesterol-rich LDL and an increase in the level of triglyceride-rich particles.
“LDLR deficiency leads to a large increase in levels of apoB-100-bearing cholesterol-rich LDL and an increase in the level of triglyceride-rich particles (49), whereas inactivation of LRP1 in the liver (15) or systemic inactivation of LRP5 has no effect on lipoprotein clearance under normal physiological conditions (58).”
From Liver heparan sulfate proteoglycans mediate clearance of triglyceride-rich lipoproteins independently of LDL receptor family members (2007) · cites this paper as [49]
Serum cholesterol is much higher in LDLR-null than in arh-deleted mice.
“serum cholesterol is much higher in LDLR-null than in arh-deleted mice”
From Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol (2016) · cites this paper as [25]
More than 95% of the adenovirus is cleared by the liver, leading to hepatic-specific expression of syndecan-1.
“Under these conditions, more than 95% of the adenovirus is cleared by the liver (29), leading to hepatic-specific expression of syndecan-1.”
From Syndecan-1 is the primary heparan sulfate proteoglycan mediating hepatic clearance of triglyceride-rich lipoproteins in mice (2009) · cites this paper as [29]
This model is superior to previous hypercholesterolaemic models in which mice were only deficient in LDLRs, that had only mildly elevated LDL cholesterol levels and little atherosclerosis, or that were based exclusively on the overexpression of apoB100 and no alteration in plasma total cholesterol.
“This model is superior to previous hypercholesterolaemic models in which mice were only deficient in LDLRs, that had only mildly elevated LDL cholesterol levels and little atherosclerosis [27], or that were based exclusively on the overexpression of apoB100 and no alteration in plasma total cholesterol [28].”
From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [27]
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Cites
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Metadata
- Authors
- Ishibashi, S., Brown, M. S., Goldstein, J. L., Gerard, R. D., Hammer, R. E., & Herz, J.
- Venue
- Journal of Clinical Investigation
- Published
- 1993-08-01
- Volume
- 92
- Issue
- 2
- Pages
- 883-893
- ISSN
- 0021-9738
- Cited by
- 1,354
- References
- 5
- Language
- en
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