reverse cholesterol transport

The other pathway is the HDL receptor(s)-mediated pathway. HDL has varying degrees of dysfunction reflected in impaired reverse cholesterol transport (RCT). Reverse cholesterol transport (RCT) is the term used for this extraction of unneeded cholesterol. Human plasma high-density lipoprotein cholesterol concentrations are a negative risk factor for atherosclerosis-linked cardiovascular disease. Reverse Cholesterol Transport a potential therapeutic target for atherosclerosis PROEFSCHRIFT ter verkrijging van de graad Doctor aan de Universiteit Leiden, op gezag van de Rector Magnificus Prof. mr. P.F. In addition to RCT, HDL might (1) suppress cytokine-induced adhesion of endothelial cells; (2) protect LDL from oxidation; and (3) have anticoagulant effects (21). The final step in plasma HDL metabolism involves the clearance of apo A-I and pre β-1 HDL in the kidney and excretion in the urine. Etoposide, a DNA topoisomerase II inhibitor as used in cancer chemotherapy, is an inducer of CETP via LXRα [3]. 3' educatie - 20 jan. 2016 - NLA Lipid Lessons - Prof.dr. ABCA1 is equally highly expressed in macrophages as well as in atherosclerotic lesions, where it colocalizes with cholesterol-loaded macrophages [19]. J Lipid … The ABCA-1 transporter protein facilitates the efflux of intracellular cholesterol through an interaction with apo AI on lipid-deplete HDL. Reverse cholesterol transport (RCT) is a pivotal pathway involved in the return of excess cholesterol from peripheral tissues to the liver for excretion in the bile and eventually the feces. HDL biogenesis starts with the formation of the nascent discoidal HDL through apoA-I and ABCA1, a specific transporter molecule that facilitates the transfer of phospholipids and cholesterol to apoA-I. Clin Sci (Lond). van de Peppel IP, Bertolini A, van Dijk TH, Groen AK, Jonker JW, Verkade HJ. Wat is reverse cholesterol transport? Epub 2017 Oct 26. In this paradigm, cholesterol is transferred from arterial macrophages to extracellular HDL through the action of transporters such as ATP-binding cassette transporter A1 and ATP-binding cassette transporter G1. In human plasma, small discoidal HDL is composed most exclusively of apoA-I, demonstrating that in vivo apoA-I plays a predominant role in stimulating cholesterol efflux via ABCA1 as compared to other apolipoproteins. Liver X receptor (LXR) is known as a strong nuclear factor inducing CETP gene expression. Reverse cholesterol transport is a multi-step process resulting in the net movement of cholesterol from peripheral tissues back to the liver first via entering the lymphatic system, then the bloodstream. Reverse cholesterol transport (RCT) is a pathway by which accumulated cholesterol is transported from the vessel wall to the liver for excretion, thus preventing atherosclerosis. nHDL-apo AI and some nHDL-FC and PL rapidly transfer to HDL, t. Rosales C, Gillard BK, Xu B, Gotto AM Jr, Pownall HJ. J. Chiang, in Pathobiology of Human Disease, 2014. Arterioscler Thromb Vasc Biol. Reverse cholesterol transport is a term that comprises all the different steps in cholesterol metabolism between cholesterol efflux from macrophage foam cells and the final excretion of cholesterol into the feces either as neutral sterols or after metabolic conversion into bile acids (see Figure 1) [5, 10, 11]. Reverse cholesterol transport incorporates HDL metabolism and involves the movement of cholesterol from extrahepatic tissue, including the vessel wall, to the liver for excretion.12 The HDL lipoproteins are the smallest and most dense lipid particles. The major lipoprotein components in HDL are ApoAI, ApoCII, and ApoE. Reverse cholesterol transport (RCT) is a pivotal pathway involved in the return of excess cholesterol from peripheral tissues to the liver for excretion in the bile and eventually the feces. Clipboard, Search History, and several other advanced features are temporarily unavailable. 1 and 2). 2019 Jan-Mar;15(1):47-54. doi: 10.14797/mdcj-15-1-47. The modified HDLs are then secreted back into the circulation where they can acquire further cholesterol before returning to the liver. The major apoprotein constituents of HDL are the A apoproteins (AI, AII, AIV), which are responsible for modulating HDL metabolism. Ken-ichi Hirano, ... Yuji Matsuzawa, in Encyclopedia of Endocrine Diseases, 2004. Reverse cholesterol transport ABC-transporter A1 Scavenger receptor class B type I: Abstract: Atherosclerosis is the major cause of death in the Western society due to the development of acute clinical events such as myocardial infarction and cerebral stroke. Altered composition and functional profile of high-density lipoprotein in leprosy patients. ApoCII is the major ApoC in HDL, and is an activator of LPL. Robert A. Hegele, in Emery and Rimoin's Principles and Practice of Medical Genetics, 2013. Although bone marrow transplantation studies revealed that macrophage does not represent a predominant source of circulating HDL-C [20], inactivation of ABCA1 in macrophages results in a marked increase in atherosclerotic lesion development [21]. This is the process whereby, as the HDL particles move through the circulation, they extract free cholesterol from less-dense particles throughout the circulatory tree, thereby reducing the overall level of total cholesterol. Bioloog Arne Dikkers onderzocht de verschillende stappen in dit proces. In the latter pathway, cholesteryl esters can be exchanged for triglycerides in apoB-rich particles (LDL and VLDL) by cholesteryl ester transfer protein (CETP). Rejuvenation Res. The scavenger receptor class B1 (SR-B1) modulates the selective uptake of HDL cholesterol ester by hepatocytes. Mechanisms to increase reverse cholesterol transport (RCT) and biliary sterol disposal are currently sought to prevent atherosclerosis. Cholesterol from non-hepatic peripheral tissues is transferred to HDL by the ABCA1 ( ATP-binding cassette transporter ). Sluiten. pre-β-HDL is a nascent, discoid particle that is ApoA-rich and lipid poor. Impairment of RCT due to dysfunctional or reduced HDL has been observed, among others, in the elderly and subjects with CAD, diabetes and Alzheimer's disease (Clee et al., 2000; Singh-Manoux et al., 2008). J Lipid Res. The effects on lipoprotein profiles of estrogen, various estrogen/progestin combinations, and selective estrogen receptor modulators (SERMs) are qualitatively generally similar but differ quantitatively. The ABCA1 transporter ensures the efflux of free cholesterol and phospholipids to nonlipidated apolipoproteins allowing genesis of nascent discoidal HDL [14]. Related terms: Macrophage; Macrophages 2) LCAT catalyzes the conversion of FC to CE, which forms a central core within spherical HDL. ABCA1-expressing cells extrude FC and PL via the interaction of apo AI with ABCA1 giving nHDL (1). Fig1: The reverse cholesterol transport pathway delivers free cholesterol from macrophages or other cells to the liver or intestine for excretion. ABCA1-Derived Nascent High-Density Lipoprotein-Apolipoprotein AI and Lipids Metabolically Segregate. Pharmacological attempts to reduce atherosclerotic cardiovascular disease by increasing plasma high-density lipoprotein cholesterol have been disappointing so that recent research has shifted from HDL quantity to HDL quality, that is, functional vs dysfunctional HDL. Donate here: http://www.aklectures.com/donate.php Facebook link: https://www.facebook.com/aklectures Website link: http://www.aklectures.com SR-B1 mediates the selective uptake of cholesterol ester and other lipids. In addition to plasma lipid transfer/exchange activity, CETP may have an intracellular function of interorganelle cytosolic lipid transfer activity. In addition to apoA-I, plasma HDLs also contain many other apolipoproteins, including apoC-II and apoE. Thus in circumstances leading to lower LDL-C levels, CETP activators may be beneficial for atherosclerosis prevention. The liver and intestine synthesize and secrete nascent discoid HDL, which consists mainly of apo E, apo Cs, phospholipids, and free cholesterol. van der Heijden, volgens besluit van het College voor Promoties te verdedigen op dinsdag 1 november 2011 klokke 15.00 uur door Ying Zhao Xu B, Gillard BK, Gotto AM Jr, Rosales C, Pownall HJ. Cholesterol ester is hydrolyzed by cholesterol ester esterase and secreted as biliary cholesterol or utilized to produce steroid hormones. In the plasma, apoA-I activates the enzyme lecithin–cholesterol acyltransferase, which converts discoidal HDL to mature, spherical, cholesteryl ester-rich HDL particles by drawing free cholesterol and phospholipids from IDLs and LDLs until spherical HDL particles are formed with a surface coat of phospholipid, free cholesterol, and apolipoproteins. Data from the ERA study [NEJM (2000), 343, 522-529] of 309 women with CAD. Following this, LCAT catalyzes the esterification of HDL cholesterol (and the hydrophobicity of the sterol-ester results in its relocation from the surface of the lipoprotein to the hydrophobic core of the particle). ApoD anchors LCAT to pre-β-HDL and activates LCAT, which transfers a fatty acid from the C2-position of lecithin to the 3-hydroxy group of cholesterol to form CE. SR-B1-/- mice, which have impaired trans-hepatic FC transport, are characterized by high plasma levels of a dysfunctional FC-rich HDL that increases plasma FC bioavailability in a way that produces whole-body hypercholesterolemia and multiple pathologies. eCollection 2020 Mar. This heterogeneous population can be divided into two subclasses by ultracentrifugation: HDL2 (1.063 to 1.125 g/mL) and HDL3 (1.125 to 1.21 g/mL). In many tissues, ATP-binding cassette A1 plays a key role in efflux of cholesterol and phospholipids from liver, intestine and macrophages to pre-β-HDL and HDL. Lipoprotein distribution and serum concentrations of 7α-hydroxy-4-cholesten-3-one and bile acids: effects of monogenic disturbances in high-density lipoprotein metabolism. Efficient reabsorption of transintestinally excreted cholesterol is a strong determinant for cholesterol disposal in mice. The process is regulated by enzymes such as lecithin-cholesterol acyltrans (LCAT) and cholesterol ester transfer protein (CETP). Flores-Castillo C, Luna-Luna M, Carreón-Torres E, López-Olmos V, Frías S, Juárez-Oropeza MA, Franco M, Fragoso JM, Vargas-Alarcón G, Pérez-Méndez Ó. Int J Mol Sci. Elevation of nonfasting triglyceride (TG) levels above 1.8 g/L (2 mmol/L) is associated with increased risk of cardiovascular diseases. 2019 May 22;20(10):2521. doi: 10.3390/ijms20102521. Methodist Debakey Cardiovasc J. Hij stelde onder andere vast dat de dunne darm mogelijk bijdraagt aan het proces reverse cholesterol transport: door de uitscheiding van cholesterol uit het bloed afkomstig van de levercellen. Wouter Jukema. The response of HDL-C to SSR may be augmented in women with specific ER-α polymorphisms (i.e., IVS1-401 C/C). The liver and intestine both significantly contribute to apoA-I synthesis and secretion, with hepatic and intestinal ABCA1 accounting for 90% and 50%, respectively, of circulating plasma apoA-I levels [15,16]. This transporter protein regulates the concentration of plasma HDL and the levels of intracellular cholesterol. Quantification of dynamic flux through the macrophage RCT pathway, although methodologically challenging, would be immensely valuable to the assessment of HDL metabolism in the setting of pharmacotherapy. See this image and copyright information in PMC. HDLs are a complex group of diverse lipoproteins that can contain many different protein constituents and carry out diverse functions related to the return of cholesterol: secretion of cholesterol from the cells, esterification of cholesterol in the plasma, transfer of cholesterol to other lipoproteins, and return of cholesterol from the peripheral tissues to the liver for excretion in the bile. HDL, high-density lipoprotein; LDL, low-density lipoprotein; TG, triglyceride. The gatekeeper of RCT and HDL generation is an ATP-binding cassette transporter called ABCA1. In the context of atheroprotection, RCT occurs by 2 mechanisms: one is the well-known trans-hepatic pathway comprising macrophage free cholesterol (FC) efflux, which produces early … Attie AD, Kastelein JP, Hayden MR: Pivotal role of ABCA1 in reverse cholesterol transport influencing HDL levels and susceptibility to atherosclerosis. HDL particles are heterogeneous. Nascent HDL particles (Figure 96-1) attract excess free cholesterol from both extrahepatic cells and other circulating lipoproteins. The particle acquires apo A proteins, which provides the lipoprotein with the capacity to utilize LCAT and adenosine triphosphate-binding cassette protein A1 (ABCA-1). Cholesterol Efflux and Reverse Cholesterol Transport 185. Hepatic Overexpression of Endothelial Lipase Lowers High-Density Lipoprotein but Maintains Reverse Cholesterol Transport in Mice: Role of Scavenger Receptor Class B Type I/ATP-Binding Cassette Transporter A1-Dependent Pathways. HDL-C is considered "good cholesterol" because of the physiologic function it performs in "reverse cholesterol transport." The uptake of apoB-rich particles via hepatic LDL receptors enables the delivery of cholesterol to the liver (approximately 50% of RCT). A Video navigatie menu. Menu en zoeken; Contact; My University; Student Portal Reverse cholesterol transport (RCT) is the process by which high-density lipoproteins (HDL) are able to extract excess cholesterol from blood vessel walls and deliver it back to the liver and gastrointestinal tract for disposal (Figure). HDL has varying degrees of dysfunction reflected in impaired reverse cholesterol transport (RCT). They can also be separated according to protein content using immunological assays (23); these specialized methods are beyond the reach of most clinical laboratories. In research laboratories, HDL particles can be subfractionated according to size and density by ultracentrifugation and gradient electrophoresis (22). ApoE is a high-affinity ligand for binding of CM remnant and IDL to LDL receptor, LRPs, and ApoE receptor. The initial step in HDL metabolism involves the formation of small lipid-poor nascent HDL particles in the liver and small intestine. HDL complexes with SR-B1 and is endocytosed. Ian S. Young, Brona V. Loughrey, in Comprehensive Hypertension, 2007. HDL2 is TG-rich, less dense than HDL3, and is protective against atherosclerosis, whereas HDL3 is cholesterol rich and is less protective than HDL2. Please enable it to take advantage of the complete set of features! COVID-19 is an emerging, rapidly evolving situation. ATP‐binding cassette A1 (ABCA1) on macrophages promotes phospholipid and CE onto pre‐β‐HDL particles, whereas ATP‐binding cassette G1 … A reduction of triglyceride (TG) storage was shown in CETP-overexpressing SW872 adipocytes, which is compatible with a small, active adipocyte phenotype [5]. Alternatively, CETP promotes the transfer of cholesterol ester from HDL to the apo-B-containing lipoproteins in exchange for triglyceride, yielding a small and more dense HDL particle. Revisiting Reverse Cholesterol Transport in the Context of High-Density Lipoprotein Free Cholesterol Bioavailability. HDL and Reverse Cholesterol Transport Mechanisms Under Physiological Conditions One of the antiatherogenic effects of HDL has been attributed to its function in macrophage reverse cholesterol transport (RCT), i.e., the removal of excess cholesterol from lipid-laden macrophage foam cells in the atherosclerotic plaque and its transport to the liver for excretion in the bile (Rader 2006). This indicates that efficient ABCA1-mediated macrophage cholesterol efflux is required to prevent excessive accumulation of cholesterol in macrophages located within the arterial wall and their subsequent transformation into foam cells. Een beter begrip van reverse cholesterol transport kan waarschijnlijk helpen in de behandeling en de preventie van hart- en vaatziekten. Cellular cholesterol efflux is mediated by HDL, acting in conjunction with the cholesterol esterifying enzyme, lecithin: cholesterol acyltransferase. Lipid-rich HDLs can enter the hepatocytes through an apoA-I receptor, where it can transfer cholesterol and cholesterol esters to distinct pools within the cell. The main lipoprotein involved in this process is the HDL-c. First, the intestine and liver synthesize the protein Apo A-1 (70% of the protein content of HDL-c), which enters the bloodstream and goes to peripheral tissues (e.g., heart). 2020 Mar 30;14(3):e0008138. HDL particles acquire ApoE and ApoCII from VLDL CM via CETP. CETP could promote reverse cholesterol transport as long as the LDL receptor and other receptors are upregulated as shown in transgenic mice. Here we describe a simplified version of reverse cholesterol transport, how this has been modified by new research into HDL, and we explain the effect of raising or lowering insulin and insulin sensitivity on RCT. The receptor, present on hepatocytes, binds to HDL and other lipoproteins, mediating the transfer of cholesterol from serum HDL to the bile for excretion, completing the cycle of RCT and removal of cholesterol from the body (20). Through this cycle, HDL mediates the delivery of cholesterol to the liver where it is metabolized and excreted into bile (Singh et al., 2007). We have used combinatorial chemistry and structure-based drug design to develop a potent and subtype-selective PPARδ agonist, GW501516. A. Hegele, in the HDL Handbook, 2010 beter begrip van cholesterol... 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