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https://www.readbyqxmd.com/read/29244772/sphingosine-1-phosphate-receptor-1-expressed-in-myeloid-cells-slows-diet-induced-atherosclerosis-and-protects-against-macrophage-apoptosis-in-ldlr-ko-mice
#1
Leticia Gonzalez, Alexander S Qian, Usama Tahir, Pei Yu, Bernardo L Trigatti
We generated myeloid specific sphingosine-1-phosphate receptor 1 (S1pr1) deficient mice by crossing mice that had myeloid specific expression of Cre recombinase (lyzMCre) with mice having the S1pr1 gene flanked by loxP recombination sites. We transplanted bone marrow from these mice and control lyzMCre mice with intact macrophage S1pr1 gene expression into low-density lipoprotein (LDL) receptor gene (Ldlr) deficient mice. The resulting chimeras were fed a high fat atherogenic diet for nine or twelve weeks and evaluated for atherosclerosis development in the aortic sinus...
December 15, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29235977/proprotein-convertase-subtilisin-kexin-type-9-inhibits-hepatitis-c-virus-replication-through-interacting-with-ns5a
#2
Zhubing Li, Qiang Liu
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a serine protease actively involved in regulating lipid homeostasis. Although PCSK9 has been shown to inhibit hepatitis C virus (HCV) entry and replication, the underlying mechanisms have not been thoroughly characterized. Moreover, whether PCSK9 regulates HCV translation and assembly/secretion has not been determined. We therefore further studied the effects of PCSK9 on the HCV life cycle. We showed that PCSK9 did not affect HCV translation or assembly/secretion...
December 13, 2017: Journal of General Virology
https://www.readbyqxmd.com/read/29233637/compound-heterozygous-familial-hypercholesterolemia-in-a-chinese-boy-with-a-de%C3%A2-novo-and-transmitted-low-density-lipoprotein-receptor-mutation
#3
Yizhe Ma, Yingyun Gong, Abhimanyu Garg, Hongwen Zhou
BACKGROUND: Homozygous familial hypercholesterolemia is characterized by extremely elevated serum low-density lipoprotein cholesterol (LDL-C) levels and increased risk of cardiovascular complications due to biallelic mutations in LDL receptor (LDLR). OBJECTIVE: We present a 10-year-old Chinese homozygous familial hypercholesterolemia boy with biallelic LDLR mutations including an extremely rare de novo mutation. METHODS: Detailed family history and clinical and biochemical data were gathered from the pedigree...
October 26, 2017: Journal of Clinical Lipidology
https://www.readbyqxmd.com/read/29228028/a-novel-indel-variant-in-ldlr-responsible-for-familial-hypercholesterolemia-in-a-chinese-family
#4
Hongyan Shu, Jingwei Chi, Jing Li, Wei Zhang, Wenshan Lv, Jie Wang, Yujie Deng, Xu Hou, Yangang Wang
Familial hypercholesterolemia (FH) is an inherited disorder characterized by elevation of serum cholesterol bound to low-density lipoprotein. Mutations in LDLR are the major factors responsible for FH. In this study, we recruited a four-generation Chinese family with FH and identified the clinical features of hypercholesterolemia. All affected individuals shared a novel indel mutation (c.1885_1889delinsGATCATCAACC) in exon 13 of LDLR. The mutation segregated with the hypercholesterolemia phenotype in the family...
2017: PloS One
https://www.readbyqxmd.com/read/29225464/apolipoprotein-e3-mediated-cellular-uptake-of-reconstituted-high-density-lipoprotein-bearing-core-3-10-or-17-nm-hydrophobic-gold-nanoparticles
#5
Skylar T Chuang, Young-Seok Shon, Vasanthy Narayanaswami
We have developed a high-density lipoprotein (HDL)-based platform for transport and delivery of hydrophobic gold nanoparticles (AuNPs). The ability of apolipoprotein E3 (apoE3) to act as a high-affinity ligand for the low-density lipoprotein receptor (LDLr) was exploited to gain entry of HDL with AuNPs into glioblastoma cells. AuNPs of 3, 10, and 17 nm diameter, the latter two synthesized by phase transfer process, were solubilized by integration with phospholipids and apoE3, yielding reconstituted HDL (rHDL) bearing AuNPs...
2017: International Journal of Nanomedicine
https://www.readbyqxmd.com/read/29219151/familial-hypercholesterolaemia
#6
REVIEW
Joep C Defesche, Samuel S Gidding, Mariko Harada-Shiba, Robert A Hegele, Raul D Santos, Anthony S Wierzbicki
Familial hypercholesterolaemia is a common inherited disorder characterized by abnormally elevated serum levels of low-density lipoprotein (LDL) cholesterol from birth, which in time can lead to cardiovascular disease (CVD). Most cases are caused by autosomal dominant mutations in LDLR, which encodes the LDL receptor, although mutations in other genes coding for proteins involved in cholesterol metabolism or LDLR function and processing, such as APOB and PCSK9, can also be causative, although less frequently...
December 7, 2017: Nature Reviews. Disease Primers
https://www.readbyqxmd.com/read/29216392/dioxin-like-pcb-126-increases-systemic-inflammation-and-accelerates-atherosclerosis-in-lean-ldl-receptor-deficient-mice
#7
Michael C Petriello, J Anthony Brandon, Jessie Hoffman, Chunyan Wang, Himi Tripathi, Ahmed Abdel-Latif, Xiang Ye, Xiangan Li, Liping Yang, Eun Lee, Sony Soman, Jazmyne Barney, Banrida Wahlang, Bernhard Hennig, Andrew J Morris
Exposure to dioxins and related persistent organic pollutants likely contributes to cardiovascular disease (CVD) risk through multiple mechanisms including the induction of chronic inflammation. Epidemiological studies have shown that leaner individuals may be more susceptible to the detrimental effects of lipophilic toxicants because they lack large adipose tissue depots that can accumulate and sequester these pollutants. This phenomenon complicates efforts to study mechanisms of pollutant-accelerated atherosclerosis in experimental animal models where high-fat feeding and adipose expansion limit the bioavailability of lipophilic pollutants...
December 1, 2017: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/29213121/the-genetic-spectrum-of-familial-hypercholesterolemia-fh-in-the-iranian-population
#8
R H Fairoozy, M Futema, R Vakili, M R Abbaszadegan, S Hosseini, M Aminzadeh, H Zaeri, M Mobini, S E Humphries, A Sahebkar
Familial hypercholesterolemia (FH) is an autosomal dominant disorder associated with premature cardiovascular disease (CVD). Mutations in the LDLR, APOB, and PCSK9 genes are known to cause FH. In this study, we analysed the genetic spectrum of the disease in subjects from the Iranian population with a clinical diagnosis of FH. Samples were collected from 16 children and family members from five different cities of Iran. Probands were screened for mutations in the LDLR, APOB, and PCSK9 genes using next generation sequencing, with results confirmed by Sanger sequencing...
December 6, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29210646/pcsk9-and-hypercholesterolemia-therapeutical-approach
#9
Milan Obradovic, Bozidarka Zaric, Emina Sudar-Milovanovic, Branislava Ilincic, Milan Perovic, Edita Stokic, Esma Isenovic
Despite the intensive research and progress in modern pharmacotherapy, hypercholesterolemia and related cardiovascular complications remain one of the leading causes of mortality and disability in the modern world. A significant contribution to the treatment of hypercholesterolemia was made by the discovery of proprotein convertase subtilisin/kexin type 9 (PCSK9). This enzyme is responsible for the degradation of the low-density lipoprotein (LDL) receptor (LDLR) found at the surface of the plasma membrane in the liver and directly associated with serum LDL level...
December 4, 2017: Current Drug Targets
https://www.readbyqxmd.com/read/29209403/lipid-lowering-interventions-targeting-proprotein-convertase-subtilisin-kexin-type-9-pcsk9-an-emerging-chapter-in-lipid-lowering-therapy
#10
REVIEW
Constantine E Kosmas, Eddy DeJesus, Rosmery Morcelo, Frank Garcia, Peter D Montan, Eliscer Guzman
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a serine protease that is mainly expressed in the liver but can also be found in the intestine and kidneys. PCSK9 promotes the degradation of low density lipoprotein receptors (LDLR) by reducing their recycling and targeting the receptors for lysosomal destruction, thereby decreasing the rate of removal of LDL-cholesterol from the circulation. Thus, interventions targeting PCSK9 by reducing its expression may lead to significant reductions of LDL-cholesterol and possibly decrease cardiovascular risk...
2017: Drugs in Context
https://www.readbyqxmd.com/read/29208678/microrna-100-suppresses-chronic-vascular-inflammation-by-stimulation-of-endothelial-autophagy
#11
Franziska Pankratz, Catherine Hohnloser, Xavier Bemtgen, Caterina Jaenich, Sheena Kreuzaler, Imo E Hoefer, Gerard Pasterkamp, Justin Mastroianni, Robert Zeiser, Christian Smolka, Laura A Schneider, Julien Martin, Maike Juschkat, Thomas Helbing, Martin Moser, Christoph Bode, Sebastian Grundmann
Rationale: The interaction of circulating cells within the vascular wall is a critical event in chronic inflammatory processes such as atherosclerosis, but the control of the vascular inflammatory state is still largely unclear. Objective: This study was undertaken to characterize the function of the endothelial-enriched microRNA miR-100 during vascular inflammation and atherogenesis. Methods and Results: Based on a transcriptome analysis of endothelial cells after miR-100 overexpression, we identified miR-100 as potent suppressor of endothelial adhesion molecule expression, resulting in attenuated leukocyte-endothelial interaction in vitro and in vivo as shown by flow cytometry and intravital imaging approach...
December 5, 2017: Circulation Research
https://www.readbyqxmd.com/read/29208426/5-azacytidine-engages-an-ire1%C3%AE-egfr-erk1-2-signaling-pathway-that-stabilizes-the-ldl-receptor-mrna
#12
Nourhen Mnasri, Maya Mamarbachi, Bruce G Allen, Gaétan Mayer
Hepatic low-density lipoprotein receptor (LDLR) is the primary conduit for the clearance of plasma LDL-cholesterol and increasing its expression represents a central goal for treating cardiovascular disease. However, LDLR mRNA is unstable and undergoes rapid turnover mainly due to the three AU-rich elements (ARE) in its proximal 3'-untranslated region (3'-UTR). Herein, our data revealed that 5-azacytidine (5-AzaC), an antimetabolite used in the treatment of myelodysplastic syndrome, stabilizes the LDLR mRNA through a previously unrecognized signaling pathway resulting in a strong increase of its protein level in human hepatocytes in culture...
December 2, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29204877/how-multi-scale-structural-biology-elucidated-context-dependent-variability-in-ectodomain-conformation-along-with%C3%A2-the-ligand-capture-and-release-cycle-for-ldlr-family-members
#13
REVIEW
Terukazu Nogi
The low-density lipoprotein receptor (LDLR) and its homologs capture and internalize lipoproteins into the cell. Due to the fact that LDLR family members possess a modular ectodomain that undergoes dynamic conformational changes, multi-scale structural analysis has been performed so as to understand the ligand capture and release mechanism. For example, crystallographic analyses have provided models for both the entire ectodomain and high-resolution structures of individual modules. In addition, nuclear magnetic resonance spectroscopic analyses have shown the rigidity and flexibility of inter-module linkers to restrict the mobility of ectodomain...
December 4, 2017: Biophysical Reviews
https://www.readbyqxmd.com/read/29204218/interpreting-the-mechanism-of-apoe-p-leu167del-mutation-in-the-incidence-of-familial-hypercholesterolemia-an-in-silico-approach
#14
REVIEW
Omran Mohammed Rashidi, Fatima Amanullah H Nazar, Mohamed Nabil Alama, Zuhier Ahmed Awan
Background: Apolipoprotein E (APOE) gene is a ligand protein in humans which mediates the metabolism of cholesterol by binding to the low-density lipoprotein receptor (LDLR). P.Leu167del mutation in APOE gene was recently connected with Familial Hypercholesterolemia, a condition associated with premature cardiovascular disease. The consequences of this mutation on the protein structure and its receptor binding capacity remain largely unknown. Objective: The current study aims to further decipher the underlying mechanism of this mutation using advanced software-based algorithms...
2017: Open Cardiovascular Medicine Journal
https://www.readbyqxmd.com/read/29197606/elevated-plasma-levels-of-ldl-cholesterol-promote-dissecting-thoracic-aortic-aneurysms-in-angiotensin-ii-induced-mice
#15
Hiroki Tanaka, Yasunori Iida, Takayuki Iwaki, Yuko Suzuki, Hideto Sano, Chiharu Miyajima, Nobuhiro Zaima, Takeshi Sasaki, Ayato Sumioka, Shogo Hakamata, Hideyuki Shimizu, Kazuo Umemura, Tetsumei Urano
BACKGROUND: Plasma low-density lipoprotein (LDL)-cholesterol is implicated in aortic aneurysm (AA) and dissection (AD); however, its role in the pathogenesis of AA and AD, a disease with a high mortality rate, is unknown. The existing animal models such as apolipoprotein E-deficient (Apoe-/-) mice cannot reproduce all the conditions of AA/AD, including elevated LDL-cholesterol levels and spontaneous atheroma formation; therefore, a more reliable in vivo model is required. Here, we analyzed angiotensin II-induced mice with combined deficiency of the LDL receptor and the catalytic component of the apolipoprotein B-edisome complex (Ldlr-/-/Apobec1-/-) to understand AA formation and AD occurrence in relation to plasma lipid composition...
November 29, 2017: Annals of Vascular Surgery
https://www.readbyqxmd.com/read/29191921/selective-egfr-epidermal-growth-factor-receptor-deletion-in-myeloid-cells-limits-atherosclerosis
#16
Lynda Zeboudj, Andréas Giraud, Lea Guyonnet, Yujiao Zhang, Ludivine Laurans, Bruno Esposito, Jose Vilar, Anna Chipont, Nikolina Papac-Milicevic, Christoph J Binder, Alain Tedgui, Ziad Mallat, Pierre-Louis Tharaux, Hafid Ait-Oufella
OBJECTIVE: To determine the consequences of specific inhibition of EGFR (epidermal growth factor receptor) in myeloid cells in atherosclerosis development. APPROACH AND RESULTS: Atherosclerotic lesion size was significantly reduced in irradiated Ldlr-/- mice reconstituted with LysMCre+Egfrlox/lox bone marrow, compared with chimeric Ldlr-/- mice reconstituted with LysMCre-Egfrlox/lox bone marrow, after 4 (-43%; P<0.05), 7 (-34%; P<0.05), and 12 weeks (-54%; P<0...
November 30, 2017: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/29190549/cholesterol-oversynthesis-markers-define-familial-combined-hyperlipidemia-versus-other-genetic-hypercholesterolemias-independently-of-body-weight
#17
Lucía Baila-Rueda, Ana Cenarro, Itziar Lamiquiz-Moneo, Sofía Perez-Calahorra, Ana M Bea, Victoria Marco-Benedí, Estíbaliz Jarauta, Rocío Mateo-Gallego, Fernando Civeira
Primary hypercholesterolemia of genetic origin, negative for mutations in LDLR, APOB, PCSK9 and APOE genes (non-FH GH), and familial combined hyperlipidemia (FCHL) are polygenic genetic diseases that occur with hypercholesterolemia, and both share a very high cardiovascular risk. In order to better characterize the metabolic abnormalities associated with these primary hypercholesterolemias, we used noncholesterol sterols, as markers of cholesterol metabolism, to determine their potential differences. Hepatic cholesterol synthesis markers (desmosterol and lanosterol) and intestinal cholesterol absorption markers (sitosterol and campesterol) were determined in non-FH GH (n=200), FCHL (n=100) and genetically defined heterozygous familial hypercholesterolemia subjects (FH) (n=100) and in normolipidemic controls (n=100)...
November 27, 2017: Journal of Nutritional Biochemistry
https://www.readbyqxmd.com/read/29190422/structure-specific-effects-of-short-chain-fatty-acids-on-plasma-cholesterol-concentration-in-male-syrian-hamsters
#18
Yimin Zhao, Jianhui Liu, Wangjun Hao, Hanyue Zhu, Ning Liang, Zouyan He, Ka Ying Ma, Zhen-Yu Chen
Previous studies have shown that short-chain fatty acids (SCFAs) are capable of decreasing plasma cholesterol. However, the relative plasma cholesterol-lowering activity of individual SCFAs and the underlying mechanisms by which SCFAs decrease plasma cholesterol remain largely unknown. The present study was to compare plasma cholesterol-lowering potency of four common SCFAs with 2-5 carbons, and to investigate their interactions with gene expressions of key regulatory factors involved in cholesterol metabolism...
November 30, 2017: Journal of Agricultural and Food Chemistry
https://www.readbyqxmd.com/read/29187523/modeling-hypercholesterolemia-and-vascular-lipid-accumulation-in-ldl-receptor-mutant-zebrafish
#19
Chao Liu, Young Sook Kim, Jungsu Kim, Jennifer Pattison, Andrés Kamaid, Yury I Miller
Elevated plasma low-density lipoprotein (LDL) cholesterol is the dominant risk factor for the development of atherosclerosis and cardiovascular disease. Deficiency in the LDL receptor (LDLR) is a major cause of familial hypercholesterolemia in humans, and the LDLR knockout mouse is a major animal model of atherosclerosis. Here we report the generation and characterization of an ldlr mutant zebrafish as a new animal model to study hypercholesterolemia and vascular lipid accumulation, an early event in the development of human atherosclerosis...
November 29, 2017: Journal of Lipid Research
https://www.readbyqxmd.com/read/29183623/role-of-angiopoietin-like-3-angptl3-in-regulating-plasma-level-of-low-density-lipoprotein-cholesterol
#20
Yu-Xin Xu, Valeska Redon, Haojie Yu, William Querbes, James Pirruccello, Abigail Liebow, Amy Deik, Kevin Trindade, Xiao Wang, Kiran Musunuru, Clary B Clish, Chad Cowan, Kevin Fizgerald, Daniel Rader, Sekar Kathiresan
BACKGROUND AND AIMS: Angiopoietin-like 3 (ANGPTL3) has emerged as a key regulator of lipoprotein metabolism in humans. Homozygous loss of ANGPTL3 function causes familial combined hypolipidemia characterized by low plasma levels of triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C). While known effects of ANGPTL3 in inhibiting lipoprotein lipase and endothelial lipase contribute to the low TG and HDL-C, respectively, the basis of low LDL-C remains unclear...
September 21, 2017: Atherosclerosis
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