Understanding Changes in High Density Lipoproteins During the Acute Phase Response
2006; Lippincott Williams & Wilkins; Volume: 26; Issue: 8 Linguagem: Inglês
10.1161/01.atv.0000232522.47018.a6
ISSN1524-4636
AutoresBrian J. Van Lenten, Srinivasa T. Reddy, Mohamad Navab, Alan M. Fogelman,
Tópico(s)Paraoxonase enzyme and polymorphisms
ResumoHomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 26, No. 8Understanding Changes in High Density Lipoproteins During the Acute Phase Response Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBUnderstanding Changes in High Density Lipoproteins During the Acute Phase Response Brian J. Van Lenten, Srinivasa T. Reddy, Mohamad Navab and Alan M. Fogelman Brian J. Van LentenBrian J. Van Lenten From the Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA. , Srinivasa T. ReddySrinivasa T. Reddy From the Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA. , Mohamad NavabMohamad Navab From the Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA. and Alan M. FogelmanAlan M. Fogelman From the Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA. Originally published1 Aug 2006https://doi.org/10.1161/01.ATV.0000232522.47018.a6Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1687–1688During infection and inflammation there is a cascade of reactions that occurs in the host collectively known as the acute-phase response (APR).1 Besides alterations in acute-phase reactants (plasma proteins), the APR is also associated with changes in lipoproteins.2 Increasing evidence suggests that high density lipoproteins (HDL) are a critical part of the acute phase response (APR) of the innate immune system.3 During infection and inflammation, there is a reduction in levels of several plasma proteins involved in HDL-mediated reverse cholesterol transport and inhibiting plasma lipid oxidation, such as lecithin:cholesterol acyltransferase (LCAT), cholesterol ester transfer protein, phospholipid transfer protein, hepatic lipase, apolipoprotein A-I (apoA-I), and paraoxonase (PON).2 Moreover, the composition of circulating HDL during an APR, also known as acute-phase HDL, is altered. Analysis of the lipid composition shows that acute-phase HDL is depleted in cholesterol ester but enriched in free cholesterol, triglyceride, and free tty acids.4 Changes in the phospholipid content of acute-phase HDL was shown to be more variable, having increased in one study5 but decreased in another.6 The levels of apolipoprotein J (apoJ or clusterin) and serum amyloid A (SAA) increase several fold in acute-phase HDL.7 Because of the marked changes in HDL during an APR, acute-phase HDL behaves differently from normal HDL in terms of its protective effect against atherosclerosis.8 Malle and coworkers have shown that acute-phase HDL was less effective in removing cholesterol from macrophages.9 Delivery of cholesterol ester to hepatocytes is also decreased during an APR because of changes in HDL composition and a reduction in hepatic scavenger receptor class B type.10See page 1806A protective role for HDL in atherogenesis likely relates, in part, to antioxidant enzymes associated with it. PON has been shown to be effective in preventing metal ion–dependent oxidation of LDL and can protect against LDL oxidation in vitro.11,12 PON is also capable of destroying the biologically active lipids that are generated in LDL when LDL becomes trapped in an artery wall cell coculture system and may function similarly in the vessel wall in vivo.11,12 In rabbits, Van Lenten reported that the APR resulted in apoA-I being displaced from HDL by SAA, which was associated with a decrease in PON activity and the conversion of HDL to a proinflammatory state.7 Kisilevsky et al13 postulated that the principal role for SAA in acute inflammation is to enhance cholesterol removal from sites of tissue destruction, whereas Gonnermann et al14 proposed that SAA enrichment of HDL during the acute-phase response may cause HDL to deliver phospholipids and cholesterol to cells involved in tissue repair at sites of inflammation. In reviewing the changes in HDL induced by the APR, Khovidhunkit15 et al commented, "Because apoSAA can displace apoA-I from HDL16,17 and apoSAA-rich HDL particles are rapidly cleared from the circulation,18 it has been assumed that the several-fold increase in apoSAA content in HDL is the mechanism for the decrease in apoA-I and HDL levels. However, we have shown that the decrease in HDL is very rapid, occurring before the increase in SAA.19 Furthermore, a study in mice in which apoSAA levels were markedly increased to levels comparable to those seen in infection found no changes in HDL cholesterol or apoA-I levels.20 Thus, high levels of SAA per se do not decrease HDL or apoA-I levels in the absence of the other changes that occur during infection and inflammation."The notion that displacement of apoA-I from HDL during an APR may contribute to a less protective form of HDL was advanced by evidence from Burger and colleagues, who demonstrated an inhibition of cellular contact between stimulated T cells and monocytes by HDL-associated apoA-I.21 This mechanism inhibits monocyte activation and therefore both tumor necrosis factor (TNF)-α and interleukin (IL)-1β production. Noting that this inhibitory activity is present in plasma, the authors suggest that apoA-I controls the contact-mediated activation of monocytes in the blood stream. By inhibiting contact-mediated activation of monocytes, HDL-associated apoA-I displays antiinflammatory properties in a mechanism relevant to atherosclerosis.In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology Han et al22 demonstrate in an elegant series of in vitro and in vivo studies reciprocal and coordinate regulation of serum amyloid A versus apoA-I and PON-1 by inflammation in murine hepatocytes. These authors convincingly demonstrate that cytokines coordinately increase SAA and decrease apoA-I and PON-1. These reciprocal changes appear to be promoted by NF-κB and repressed by the nuclear receptor PPAR-α. As the authors note, neither apoA-I nor PON-1 promoters contain NF-κB sites,23–26 and the SAA promoters do not contain PPAR response elements.27 Thus, the mechanism for this coordinate regulation may be indirect both for PPAR-α and NF-κB. Despite the absence of a clear mechanism for the all the steps involved, their experiments in PPAR-α–deficient mice convincingly demonstrate that PPAR-α does affect the expression of mouse apoA-I, and shows that PPARα activation can mitigate NF-κB activation by inflammatory stimuli.The authors propose a model whereby reciprocal changes during cytokine-mediated inflammation are regulated by an interaction between PPAR-α and NF-κB, inducing counter-regulatory transcriptional responses through changes in expression of their target genes. Their work also suggests that PPAR-α expression exerts a chronic "braking" effect on inflammation, which can be reversed by inflammatory cytokines or the absence of PPAR-α itself.These studies22 together with the earlier studies19,20 suggest that the reduction in apoA-I and PON during the APR is most likely not simply attributable to the displacement of apoA-I particles containing PON by SAA but is an example of the extraordinary molecular complexity of the APR, which includes reciprocal and coordinate changes of many important proteins.DisclosuresMN, STR, and AMF are principals in Bruin Pharma and AMF is an officer in Bruin Pharma.FootnotesCorrespondence to Brian J. Van Lenten, PhD, Room BH-307 CHS, Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, Los Angeles, CA 90095-1679. E-mail [email protected] References 1 Gabay C, Kushner I. Acute-phase proteins and other systemic responses to inflammation. N Engl J Med. 1999; 340: 448–454.CrossrefMedlineGoogle Scholar2 Khovidhunkit W, Memon RA, Feingold KR, Grunfeld C. Infection and inflammation-induced proatherogenic changes of lipoproteins. J Infect Dis. 2000; 181: S462–S472.CrossrefMedlineGoogle Scholar3 Navab M, Berliner JA, Subbanagounder G, Hama S, Lusis AJ, Castellani LW, Reddy ST, Shih D, Shi W, Watson AD, Van Lenten BJ, Vora D, Fogelman AM. HDL and the inflammatory response induced by LDL-derived oxidized phospholipids. Arterioscler Thromb Vasc Biol. 2001; 21: 481–488.CrossrefMedlineGoogle Scholar4 Cabana VG, Lukens JR, Rice KS, Hawkins TJ, Getz GS. HDL content and composition in acute phase response in three species: triglyceride enrichment of HDL a factor in its decrease. J Lipid Res. 1996; 37: 2662–2674.CrossrefMedlineGoogle Scholar5 Auerbach BJ, Parks JS. Lipoprotein abnormalities associated with lipopolysaccharide (LPS)-induced lecithin: cholesterol acyltransferase and lipase deficiency. J Biol Chem. 1989; 264: 10264–10270.CrossrefMedlineGoogle Scholar6 Cabana VG, Siegel JN, Sabesin SM. Effects of the acute phase response on the concentration and density distribution of plasma lipids and apolipoproteins. J Lipid Res. 1989; 30: 39–49.CrossrefMedlineGoogle Scholar7 Van Lenten BJ, Wagner AC, Nayak DP, Hama S, Navab M, Fogelman AM. HDL loses its anti-inflammatory properties during acute influenza A infection. Circulation. 2001; 103: 2283–2288.CrossrefMedlineGoogle Scholar8 Van Lenten BJ, Hama SY, deBeer FC, Stafforini DM, McIntyre TM, Prescott SM, La Du BN, Fogelman AM, Navab M. Anti-inflammatory HDL becomes pro-inflammatory during the acute phase response. Loss of protective effect of HDL against LDL oxidation in aortic wall cell cocultures. J Clin Invest. 1995; 96: 2758–2767.CrossrefMedlineGoogle Scholar9 Artl A, Marsche G, Lestavel S, Sattler W, Malle E. Role of serum amyloid A during metabolism of acute-phase HDL by macrophages. Arterioscler Thromb Vase Biol. 2000; 20: 763–772.CrossrefMedlineGoogle Scholar10 Artl A, Marsche G, P. Pussinen P, G. Knipping G, Sattler W, Malle E. Impaired capacity of acute-phase high density lipoprotein particles to deliver cholesteryl ester to the human HUH-7 hepatoma cell line. Int J Biochem Cell Biol. 2002; 34: 370–381.CrossrefMedlineGoogle Scholar11 Watson AD, Navab M, Hama SY, Sevanian A, Prescott SM, Stafforini DM, McIntyre TM, La Du BN, Fogelman AM, Berliner JA. Effect of platelet activating factor-acetylhydrolase on the formation and action of minimally oxidized low density lipoprotein. J Clin Invest. 1995; 95: 774–782.CrossrefMedlineGoogle Scholar12 Watson AD, Berliner JA, Hama SY, La Du BN, Faull KF, Fogelman AM, Navab M. Protective effect of high density lipoprotein associated PON. Inhibition of the biological activity of minimally oxidized low density lipoprotein. J Clin Invest. 1995; 96: 2882–2891.CrossrefMedlineGoogle Scholar13 Kisilevsky R, Lindhorst E, Ancsin JB, Young D, Bagshaw W. Acute phase serum amyloid A (SAA) and cholesterol transport during acute inflammation: a hypothesis. Amyloid: Int J Exp Clin Invest. 1996; 3: 252–260.Google Scholar14 Gonnerman WA, Lim M, Sipe JD, Hayes KC, Cathcart ES. The acute phase response in Syrian hamsters elevates apolipoprotein serum amyloid A (apoSAA) and disrupts lipoprotein metabolism. Amyloid: Int J Exp Clin Invest. 1996; 3: 261–269.Google Scholar15 Khovidhunkit W, Kim M-S, Memon RA, Shigenaga JK, Moser AH, Feingold KR, Grunfeld C. Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host. J Lipid Res. 2004; 45: 1169–1196.CrossrefMedlineGoogle Scholar16 Husebekk A, Skogen B, Husby G. High-density lipoprotein has different binding capacity for different apoproteins. The amyloidogenic apoproteins are easier to displace from high density lipoprotein. Scand J Immunol. 1988; 28: 653–658.CrossrefMedlineGoogle Scholar17 Coetzee GA, Strachan AF, van der Westhuyzen DR, Hoppe HC, Jeenah MS, de Beer FC. Serum amyloid A-containing human high density lipoprotein 3. Density, size, and apolipoprotein composition J Biol Chem. 1986; 261: 9644–9651.CrossrefMedlineGoogle Scholar18 Hoffman JS, Benditt EP. Plasma clearance kinetics of the amyloid-related high density lipoprotein apoprotein, serum amyloid protein (apoSAA), in the mouse. Evidence for rapid apoSAA clearance J Clin Invest. 1983; 71: 926–934.CrossrefMedlineGoogle Scholar19 Ly H, Francone OL, Fielding CJ, Shigenaga JK, Moser AH, Grunfeld C, Feingold KR. Endotoxin and TNF lead to reduced plasma LCAT activity and decreased hepatic LCAT mRNA levels in Syrian hamsters. J Lipid Res. 1995; 36: 1254–1263.CrossrefMedlineGoogle Scholar20 Hosoai H, Webb NR, Glick JM, Tietge UJ, Purdom MS, de Beer FC, Rader DJ. Expression of serum amyloid A protein in the absence of the acute phase response does not reduce HDL cholesterol or apoA-I levels in human apoA-I transgenic mice. J Lipid Res. 1999; 40: 648–653.CrossrefMedlineGoogle Scholar21 Hyka N, Dayer J-M, Modoux C, Kohno T, Edwards CK, Roux-Lombard P, and Burger D. Apolipoprotein A-I inhibits the production of IL-1beta and tumor necrosis factor-alpha by blocking contact-mediated activation of monocytes by T lymphocytes. Blood. 2001; 97: 2381–2389.CrossrefMedlineGoogle Scholar22 Han CY, Chiba T, Campbell JS, Faust N, Chaisson M, Orasanu G, Plutzky J, Chait A. Reciprocal and co-ordinate regulation of serum amyloid A versus apolipoprotein A-I and paraoxonase-1 by inflammation in murine hepatocytes. Arterioscler Thromb Vasc Biol. 2006; 26; 1806–1813.LinkGoogle Scholar23 Staels B, Auwerx J. Regulation of apo A-I gene expression by fibrates. Atherosclerosis. 1998; 137: S19–S23.CrossrefMedlineGoogle Scholar24 Berthou L, Duverger N, Emmanuel F, Langouet S, Auwerx J, Guillouzo A, Fruchart JC, Rubin E, Denefle P, Staels B, Branellec D. Opposite regulation of human versus mouse apolipoprotein A-I by fibrates in human apolipoprotein A-I transgenic mice. J Clin Invest. 1996; 97: 2408–2416.CrossrefMedlineGoogle Scholar25 Gouedard C, Koum-Besson N, Barouki R, Morel Y. Opposite regulation of the human paraoxonase-1 gene PON-1 by fenofibrate and statins. Mol Pharmacol. 2003; 63: 945–956.CrossrefMedlineGoogle Scholar26 Gouedard C, Barouki R, Morel Y. Induction of the paraoxonase-1 gene expression by resveratrol. Arterioscler Thromb Vasc Biol. 2004; 24: 2378–2383.LinkGoogle Scholar27 Uhlar CM, Whitehead AS. Serum amyloid A, the major vertebrate acute-phase reactant. Eur J Biochem. 1999; 265: 501–523.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Ferri N, Ruscica M, Lupo M, Vicenzi M, Sirtori C and Corsini A (2022) Pharmacological rationale for the very early treatment of acute coronary syndrome with monoclonal antibodies anti-PCSK9, Pharmacological Research, 10.1016/j.phrs.2022.106439, 184, (106439), Online publication date: 1-Oct-2022. Venetsanopoulou A, Voulgari P and Drosos A (2022) Hyperlipidemia and rheumatoid arthritis Cholesterol, 10.1016/B978-0-323-85857-1.00003-1, (969-997), . Luna-Castillo K, Lin S, Muñoz-Valle J, Vizmanos B, López-Quintero A and Márquez-Sandoval F (2021) Functional Food and Bioactive Compounds on the Modulation of the Functionality of HDL-C: A Narrative Review, Nutrients, 10.3390/nu13041165, 13:4, (1165) Açıkgöz E, Açıkgöz S, Yaman B and Kurtul A (2021) Lower LDL-cholesterol levels associated with increased inflammatory burden in patients with acute ST-segment elevation myocardial infarction, Revista da Associação Médica Brasileira, 10.1590/1806-9282.67.02.20200548, 67:2, (224-229) Behl T, Kaur I, Sehgal A, Zengin G, Brisc C, Brisc M, Munteanu M, Nistor-Cseppento D and Bungau S (2020) The Lipid Paradox as a Metabolic Checkpoint and Its Therapeutic Significance in Ameliorating the Associated Cardiovascular Risks in Rheumatoid Arthritis Patients, International Journal of Molecular Sciences, 10.3390/ijms21249505, 21:24, (9505) Scavone D, Sgorbini M, Borges A, Oliveira-Filho J, Vitale V and Paltrinieri S (2020) Serial measurements of Paraoxonase-1 (PON-1) activity in horses with experimentally induced endotoxemia, BMC Veterinary Research, 10.1186/s12917-020-02629-4, 16:1, Online publication date: 1-Dec-2020. Venetsanopoulou A, Pelechas E, Voulgari P and Drosos A (2020) The lipid paradox in rheumatoid arthritis: the dark horse of the augmented cardiovascular risk, Rheumatology International, 10.1007/s00296-020-04616-2, 40:8, (1181-1191), Online publication date: 1-Aug-2020. Fawzy R, Hammad G, Egila S, Elkasas A and Fouad N (2020) Association of tumor necrosis factor-α (TNF-α) −308A/G (rs1800629) gene polymorphism with carotid artery atherosclerosis in rheumatoid arthritis patients, The Egyptian Rheumatologist, 10.1016/j.ejr.2020.05.004, 42:3, (177-181), Online publication date: 1-Jul-2020. Jagpal A and Navarro-Millán I (2018) Cardiovascular co-morbidity in patients with rheumatoid arthritis: a narrative review of risk factors, cardiovascular risk assessment and treatment, BMC Rheumatology, 10.1186/s41927-018-0014-y, 2:1, Online publication date: 1-Dec-2018. Camps J, Iftimie S, García-Heredia A, Castro A and Joven J (2017) Paraoxonases and infectious diseases, Clinical Biochemistry, 10.1016/j.clinbiochem.2017.04.016, 50:13-14, (804-811), Online publication date: 1-Sep-2017. Giordano A, Rossi G, Probo M, Moretti P and Paltrinieri S (2017) Colorimetric and electrophoretic evaluation of lipoprotein fractions in healthy neonatal calves: Comparison with results from adult cows and from calves with inflammatory conditions, Research in Veterinary Science, 10.1016/j.rvsc.2017.02.007, 111, (108-112), Online publication date: 1-Apr-2017. Sayyahfar S, Lavasani A, Nateghian A and Karimi A (2017) Evaluation of Lipid Profile Changes in Pediatric Patients with Acute Mononucleosis, Infection & Chemotherapy, 10.3947/ic.2017.49.1.44, 49:1, (44), . Cortelazzo A, De Felice C, De Filippis B, Ricceri L, Laviola G, Leoncini S, Signorini C, Pescaglini M, Guerranti R, Timperio A, Zolla L, Ciccoli L and Hayek J (2017) Persistent Unresolved Inflammation in the Mecp2 -308 Female Mutated Mouse Model of Rett Syndrome , Mediators of Inflammation, 10.1155/2017/9467819, 2017, (1-9), . Kim K, Bloom M, Browne R, Bell E, Yucel R and Fujimoto V (2016) Associations between follicular fluid high density lipoprotein particle components and embryo quality among in vitro fertilization patients, Journal of Assisted Reproduction and Genetics, 10.1007/s10815-016-0826-x, 34:1, (1-10), Online publication date: 1-Jan-2017. Pecorelli A, Cervellati C, Hayek J and Valacchi G (2016) OxInflammation in Rett syndrome, The International Journal of Biochemistry & Cell Biology, 10.1016/j.biocel.2016.07.015, 81, (246-253), Online publication date: 1-Dec-2016. González-Pacheco H, Amezcua-Guerra L, Vazquez-Rangel A, Martínez-Sánchez C, Pérez-Méndez O, Verdejo J and Bojalil R (2015) Levels of High-Density Lipoprotein Cholesterol are Associated With Biomarkers of Inflammation in Patients With Acute Coronary Syndrome, The American Journal of Cardiology, 10.1016/j.amjcard.2015.09.009, 116:11, (1651-1657), Online publication date: 1-Dec-2015. Ibba F, Rossi G, Meazzi S, Giordano A and Paltrinieri S (2015) Serum concentration of high density lipoproteins (HDLs) in leishmaniotic dogs, Research in Veterinary Science, 10.1016/j.rvsc.2014.11.011, 98, (89-91), Online publication date: 1-Feb-2015. Bag-Ozbek A and Giles J (2014) Inflammation, Adiposity, and Atherogenic Dyslipidemia in Rheumatoid Arthritis: Is There a Paradoxical Relationship?, Current Allergy and Asthma Reports, 10.1007/s11882-014-0497-6, 15:2, Online publication date: 1-Feb-2015. Tazi Mezalek Z, Harmouche H, Ammouri W, Maamar M, Adnaoui M and Cacoub P (2014) Athérosclérose au cours du lupus érythémateux systémique, La Presse Médicale, 10.1016/j.lpm.2014.01.021, 43:10, (1034-1047), Online publication date: 1-Oct-2014. Filipowicz-Sosnowska A, Głuszko P and Rupiński R (2014) Lipid profiles in rheumatoid arthritis patients treated with disease-modifying antirheumatic drugs, Rheumatology, 10.5114/reum.2014.42797, 52:2, (120-128), Online publication date: 30-Apr-2014. Cortelazzo A, De Felice C, Guerranti R, Signorini C, Leoncini S, Pecorelli A, Zollo G, Landi C, Valacchi G, Ciccoli L, Bini L and Hayek J (2014) Subclinical Inflammatory Status in Rett Syndrome, Mediators of Inflammation, 10.1155/2014/480980, 2014, (1-13), . Khoueiry G, Abdallah M, Saiful F, Abi Rafeh N, Raza M, Bhat T, El-Sayegh S, Kalantar-Zadeh K and Lafferty J (2013) High-density lipoprotein in uremic patients: metabolism, impairment, and therapy, International Urology and Nephrology, 10.1007/s11255-012-0366-y, 46:1, (27-39), Online publication date: 1-Jan-2014. Batini V and Bianchi S (2014) The CKD Patient with Dyslipidemia Dyslipidemias in Kidney Disease, 10.1007/978-1-4939-0515-7_6, (93-110), . Kassimatis T and Goldsmith D (2014) CVD in CKD: Focus on the Dyslipidemia Problem Dyslipidemias in Kidney Disease, 10.1007/978-1-4939-0515-7_5, (67-91), . Korita I, Bulo A, Langlois M, Verhoye E and Blaton V (2013) Serum amyloid A is independently related to apolipoprotein A-I but not to HDL-cholesterol in patients with angina pectoris, Clinical Biochemistry, 10.1016/j.clinbiochem.2013.07.021, 46:16-17, (1660-1663), Online publication date: 1-Nov-2013. Bazarian J, Blyth B, He H, Mookerjee S, Jones C, Kiechle K, Moynihan R, Wojcik S, Grant W, Secreti L, Triner W, Moscati R, Leinhart A, Ellis G and Khan J (2013) Classification Accuracy of Serum Apo A-I and S100B for the Diagnosis of Mild Traumatic Brain Injury and Prediction of Abnormal Initial Head Computed Tomography Scan, Journal of Neurotrauma, 10.1089/neu.2013.2853, 30:20, (1747-1754), Online publication date: 15-Oct-2013. Li Y, Kakinami C, Li Q, Yang B, Li H and Qiu J (2013) Human Apolipoprotein A-I Is Associated with Dengue Virus and Enhances Virus Infection through SR-BI, PLoS ONE, 10.1371/journal.pone.0070390, 8:7, (e70390) Kim M, de Beer M, Wroblewski J, Webb N and de Beer F (2013) SAA does not induce cytokine production in physiological conditions, Cytokine, 10.1016/j.cyto.2012.10.019, 61:2, (506-512), Online publication date: 1-Feb-2013. Otocka-Kmiecik A, Mikhailidis D, Nicholls S, Davidson M, Rysz J and Banach M (2012) Dysfunctional HDL: A novel important diagnostic and therapeutic target in cardiovascular disease?, Progress in Lipid Research, 10.1016/j.plipres.2012.03.003, 51:4, (314-324), Online publication date: 1-Oct-2012. Stancu C, Toma L and Sima A (2012) Dual role of lipoproteins in endothelial cell dysfunction in atherosclerosis, Cell and Tissue Research, 10.1007/s00441-012-1437-1, 349:2, (433-446), Online publication date: 1-Aug-2012. Kojić Z, Stojanović D and Ristić S (2012) Cholesterol, cytokines and atherosclerosis, Srce i krvni sudovi, 10.5937/siks1201002K, 31:4, (2-6), . Cavagna L, Boffini N, Cagnotto G, Inverardi F, Grosso V and Caporali R (2012) Atherosclerosis and Rheumatoid Arthritis: More Than a Simple Association, Mediators of Inflammation, 10.1155/2012/147354, 2012, (1-8), . Vaziri N, Navab K, Gollapudi P, Moradi H, Pahl M, Barton C, Fogelman A and Navab M (2011) Salutary Effects of Hemodialysis on Low-Density Lipoprotein Proinflammatory and High-Density Lipoprotein Anti-inflammatory Properties in Patient With End-Stage Renal Disease, Journal of the National Medical Association, 10.1016/S0027-9684(15)30368-0, 103:6, (524-533), Online publication date: 1-Jun-2011. Vaziri N (2010) Lipotoxicity and Impaired High Density Lipoprotein-Mediated Reverse Cholesterol Transport in Chronic Kidney Disease, Journal of Renal Nutrition, 10.1053/j.jrn.2010.05.010, 20:5, (S35-S43), Online publication date: 1-Sep-2010. Orlov S, Mogilenko D, Shavva V, Dizhe E, Ignatovich I and Perevozchikov A (2010) Effect of TNFα on activities of different promoters of human apolipoprotein A-I gene, Biochemical and Biophysical Research Communications, 10.1016/j.bbrc.2010.06.064, 398:2, (224-230), Online publication date: 1-Jul-2010. Vaziri N, Navab M and Fogelman A (2010) HDL metabolism and activity in chronic kidney disease, Nature Reviews Nephrology, 10.1038/nrneph.2010.36, 6:5, (287-296), Online publication date: 1-May-2010. Ahnström J, Gottsäter A, Lindblad B and Dahlbäck B (2010) Plasma concentrations of apolipoproteins A-I, B, and M in patients with critical limb ischemia, Clinical Biochemistry, 10.1016/j.clinbiochem.2010.01.001, 43:6, (599-603), Online publication date: 1-Apr-2010. Yang F, Yin Y, Wang F, Zhang L, Wang Y and Sun S (2009) An Altered Pattern of Liver Apolipoprotein A-I Isoforms Is Implicated in Male Chronic Hepatitis B Progression, Journal of Proteome Research, 10.1021/pr900593r, 9:1, (134-143), Online publication date: 4-Jan-2010. Schmidt O, Söderhäll K, Theopold U and Faye I (2010) Role of Adhesion in Arthropod Immune Recognition, Annual Review of Entomology, 10.1146/annurev.ento.54.110807.090618, 55:1, (485-504), Online publication date: 1-Jan-2010. Dronca M and Pasca S (2009) Paraoxonase 1 Status, Environmental Exposures, and Oxidative Stress in Autism Spectrum Disorders Autism, 10.1201/9781420068870-c6, (91-112), Online publication date: 26-Oct-2009. Lescai F, Marchegiani F and Franceschi C (2009) PON1 is a longevity gene: Results of a meta-analysis, Ageing Research Reviews, 10.1016/j.arr.2009.04.001, 8:4, (277-284), Online publication date: 1-Oct-2009. Franssen R, Sankatsing R, Hassink E, Hutten B, Ackermans M, Brinkman K, Oesterholt R, Arenas-Pinto A, Storfer S, Kastelein J, Sauerwein H, Reiss P and Stroes E (2009) Nevirapine Increases High-Density Lipoprotein Cholesterol Concentration by Stimulation of Apolipoprotein A-I Production, Arteriosclerosis, Thrombosis, and Vascular Biology, 29:9, (1336-1341), Online publication date: 1-Sep-2009. Izumi A, Yoshihara A, Hirotomi T and Miyazaki H (2009) The Relationship Between Serum Lipids and Periodontitis in Elderly Non-Smokers, Journal of Periodontology, 10.1902/jop.2009.080584, 80:5, (740-748), Online publication date: 1-May-2009. Camps J, Marsillach J and Joven J (2009) The paraoxonases: role in human diseases and methodological difficulties in measurement, Critical Reviews in Clinical Laboratory Sciences, 10.1080/10408360802610878, 46:2, (83-106), Online publication date: 1-Mar-2009. Moradi H, Pahl M, Elahimehr R and Vaziri N (2009) Impaired antioxidant activity of high-density lipoprotein in chronic kidney disease, Translational Research, 10.1016/j.trsl.2008.11.007, 153:2, (77-85), Online publication date: 1-Feb-2009. Ku I, Imboden J, Hsue P and Ganz P (2009) Rheumatoid Arthritis A Model of Systemic Inflammation Driving Atherosclerosis, Circulation Journal, 10.1253/circj.CJ-09-0274, 73:6, (977-985), . Stone N (2009) Clinical Evaluation for Genetic and Secondary Causes of Dyslipidemia Clinical Lipidology, 10.1016/B978-141605469-6.50016-0, (144-157), . Miller M (2009) High-Density Lipoprotein Cholesterol in Coronary Heart Disease Risk Assessment Clinical Lipidology, 10.1016/B978-141605469-6.50014-7, (119-129), . He Q, Yang H, Wong B and Chiu J (2008) Serological Proteomics of Gastritis: Degradation of Apolipoprotein A-I and Alpha1-Antitrypsin Is a Common Response to Inflammation Irrespective of Helicobacter pylori Infection, Digestive Diseases and Sciences, 10.1007/s10620-008-0269-z, 53:12, (3112-3118), Online publication date: 1-Dec-2008. Mak A, Ho R, Tan J, Teng G, Lahiri M, Lateef A, Vasoo S, Boey M, Koh D and Feng P (2008) Atherogenic serum lipid profile is an independent predictor for gouty flares in patients with gouty arthropathy, Rheumatology, 10.1093/rheumatology/ken471, 48:3, (262-265) Miller M (2008) Lipid Levels in the Post-Acute Coronary Syndrome Setting, Journal of the American College of Cardiology, 10.1016/j.jacc.2007.12.039, 51:15, (1446-1447), Online publication date: 1-Apr-2008. Lavie C and Milani R (2008) Shedding Light on High-Density Lipoprotein Cholesterol, Journal of the American College of Cardiology, 10.1016/j.jacc.2007.08.055, 51:1, (56-58), Online publication date: 1-Jan-2008. Deakin S and James R (2008) Transcriptional Regulation of the Paraoxonase Genes The Paraoxonases: Their Role in Disease Development and Xenobiotic Metabolism, 10.1007/978-1-4020-6561-3_16, (241-250), . Boissonneault G (2007) Dietary Fat, Immunity, and Inflammatory Disease Fatty Acids in Foods and their Health Implications,Third Edition, 10.1201/9781420006902.ch41, (977-1005), Online publication date: 19-Nov-2007. Navab M, Reddy S, Van Lenten B, Buga G, Anantharamaiah G and Fogelman A (2007) HDL and Inflammation High‐Density Lipoproteins, 10.1002/9783527625178.ch13, (339-354), Online publication date: 20-Sep-2007. Rothem L, Hartman C, Dahan A, Lachter J, Eliakim R and Shamir R (2007) Paraoxonases are associated with intestinal inflammatory diseases and intracellularly localized to the endoplasmic reticulum, Free Radical Biology and Medicine, 10.1016/j.freeradbiomed.2007.05.003, 43:5, (730-739), Online publication date: 1-Sep-2007. (2007) Case 40-2006: Anemia and Low HDL Cholesterol, New England Journal of Medicine, 10.1056/NEJMc070139, 356:18, (1893-1895), Online publication date: 3-May-2007. Hahn B, Grossman J, Chen W and McMahon M (2007) The pathogenesis of atherosclerosis in autoimmune rheumatic diseases: Roles of inflammation and dyslipidemia, Journal of Autoimmunity, 10.1016/j.jaut.2007.02.004, 28:2-3, (69-75), Online publication date: 1-Mar-2007. (2007) BIBLIOGRAPHY The Biology of Human Longevity, 10.1016/B978-012373657-4/50008-8, (417-599), . August 2006Vol 26, Issue 8 Advertisement Article InformationMetrics https://doi.org/10.1161/01.ATV.0000232522.47018.a6PMID: 16857958 Originally publishedAugust 1, 2006 PDF download Advertisement
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