Receptors, LDL

Publication Title: 
Therapeutische Umschau. Revue ThÈrapeutique

Familial forms of isolated hypercholesterolemia are inherited autosomal-dominantly and are caused by defects of the low-density lipoprotein (LDL) receptor protein or its ligand, the apolipoprotein B-100, the exclusive apolipoprotein moiety of the LDL particles. Mutations at the LDL receptor gene locus (more than 150 different mutations have been described up to now) lead to familial hypercholesterolemia (FH); the only mutation at the apolipoprotein B-100 gene locus described in detail so far leads to the so-called familial defective apolipoprotein B-100 (FDB).

Author(s): 
Miserez, A. R.
Keller, U.
Publication Title: 
The Journal of Nutrition

Glucosamine, commonly consumed for the treatment of osteoarthritis, is classified as a nutritional supplement; however, there are few data regarding its metabolic or vascular effects. Glucosamine is a component of the hexosamine pathway, which has been implicated in the development of insulin resistance. Anecdotal reports suggest that glucosamine consumption can increase circulating cholesterol concentrations.

Author(s): 
Tannock, Lisa R.
Kirk, Elizabeth A.
King, Victoria L.
LeBoeuf, Renee
Wight, Thomas N.
Chait, Alan
Publication Title: 
Journal of Lipid Research

ACAT2, the enzyme responsible for the formation of cholesteryl esters incorporated into apolipoprotein B-containing lipoproteins by the small intestine and liver, forms predominantly cholesteryl oleate from acyl-CoA and free cholesterol. The accumulation of cholesteryl oleate in plasma lipoproteins has been found to be predictive of atherosclerosis. Accordingly, a method was developed in which fatty acyl-CoA subspecies could be extracted from mouse liver and quantified.

Author(s): 
Bell, Thomas A.
Wilson, Martha D.
Kelley, Kathryn
Sawyer, Janet K.
Rudel, Lawrence L.
Publication Title: 
Arteriosclerosis, Thrombosis, and Vascular Biology

OBJECTIVES: The enzyme acyl-coenzymeA (CoA):cholesterol O-acyltransferase 2 (ACAT2) in the liver synthesizes cholesteryl esters (CE) from cholesterol and fatty acyl-CoA, which get incorporated into apoB-containing lipoproteins that are secreted into the bloodstream. Dietary fatty acid composition influences the amount and fatty acid composition of CE within apoB-containing lipoproteins.

Author(s): 
Bell, Thomas A.
Kelley, Kathryn
Wilson, Martha D.
Sawyer, Janet K.
Rudel, Lawrence L.
Publication Title: 
The Journal of Nutritional Biochemistry

We tested the hypothesis that dietary supplementation with echium oil (EO), which is enriched in stearidonic acid (SDA; 18:4 n-3), the product of Delta-6 desaturation of 18:3 n-3, will decrease plasma triglyceride (TG) concentrations and result in conversion of SDA to eicosapentaenoic acid (EPA) in the liver.

Author(s): 
Zhang, Ping
Boudyguina, Elena
Wilson, Martha D.
Gebre, Abraham K.
Parks, John S.
Publication Title: 
Circulation

BACKGROUND: Vascular inflammation and lipid deposition are prominent features of atherosclerotic lesion formation. We have shown previously that the dithiol compound alpha-lipoic acid (LA) exerts antiinflammatory effects by inhibiting tumor necrosis factor-alpha- and lipopolysaccharide-induced endothelial and monocyte activation in vitro and lipopolysaccharide-induced acute inflammatory responses in vivo.

Author(s): 
Zhang, Wei-Jian
Bird, Karyn E.
McMillen, Timothy S.
Leboeuf, Renée C.
Hagen, Tory M.
Frei, Balz
Publication Title: 
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience

Environmental and genetic factors, notably ApoE4, contribute to the etiology of late-onset Alzheimer's disease (LOAD). Reduced mRNA and protein for an apolipoprotein E (ApoE) receptor family member, SorLA (LR11) has been found in LOAD but not early-onset AD, suggesting that LR11 loss is not secondary to pathology. LR11 is a neuronal sorting protein that reduces amyloid precursor protein (APP) trafficking to secretases that generate beta-amyloid (Abeta). Genetic polymorphisms that reduce LR11 expression are associated with increased AD risk.

Author(s): 
Ma, Qiu-Lan
Teter, Bruce
Ubeda, Oliver J.
Morihara, Takashi
Dhoot, Dilsher
Nyby, Michael D.
Tuck, Michael L.
Frautschy, Sally A.
Cole, Greg M.
Publication Title: 
The Journal of Pharmacology and Experimental Therapeutics

Liver X receptor (LXR) agonists have the potential to treat atherosclerosis based on their ability to enhance reverse cholesterol transport. However, their side effects, such as induction of liver lipogenesis and triglyceridemia, may limit their pharmaceutical development.

Author(s): 
Peng, Dacheng
Hiipakka, Richard A.
Dai, Qing
Guo, Jian
Reardon, Catherine A.
Getz, Godfrey S.
Liao, Shutsung
Publication Title: 
Journal of Lipid Research

The 3'untranslated region (UTR) of human LDL receptor (LDLR) mRNA contains three AU-rich elements (AREs) responsible for rapid mRNA turnover and mediates the stabilization induced by berberine (BBR). However, the identities of the specific RNA binding proteins involved in the regulation of LDLR mRNA stability at the steady state level or upon BBR treatment are unknown.

Author(s): 
Li, Hai
Chen, Wei
Zhou, Yue
Abidi, Parveen
Sharpe, Orr
Robinson, William H.
Kraemer, Fredric B.
Liu, Jingwen
Publication Title: 
The Journal of Biological Chemistry

PCSK9 is a natural inhibitor of LDL receptor (LDLR) that binds the extracellular domain of LDLR and triggers its intracellular degradation. PCSK9 and LDLR are coordinately regulated at the transcriptional level by sterols through their promoter-imbedded sterol response elements (SRE) and co-induced by statins. Identification of regulatory networks modulating PCSK9 transcription is important for developing selective repressors of PCSK9 to improve statin efficacy by prolonging the up-regulation of LDLR.

Author(s): 
Li, Hai
Dong, Bin
Park, Sahng Wook
Lee, Hyun-Sook
Chen, Wei
Liu, Jingwen

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