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Review

Discrete roles of apoA‐I and apoE in the biogenesis of HDL species: Lessons learned from gene transfer studies in different mouse models

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Pages 14-28 | Published online: 08 Jul 2009

References

  • Zannis V. I., Chroni A., Kypreos K. E., Kan H. Y., Cesar T. B., Zanni E. E., et al. Probing the pathways of chylomicron and HDL metabolism using adenovirus‐mediated gene transfer. Curr Opin Lipidol 2004; 15: 151–66
  • Fielding C. J., Fielding P. E. Molecular physiology of reverse cholesterol transport. J Lipid Res 1995; 36: 211–28
  • Nanjee M. N., Cooke C. J., Olszewski W. L., Miller N. E. Concentrations of electrophoretic and size subclasses of apolipoprotein A‐I‐containing particles in human peripheral lymph. Arterioscler Thromb Vasc Biol 2000; 20: 2148–55
  • Acton S., Rigotti A., Landschulz K. T., Xu S., Hobbs H. H., Krieger M. Identification of scavenger receptor SR‐BI as a high density lipoprotein receptor. Science 1996; 271: 518–20
  • Stangl H., Hyatt M., Hobbs H. H. Transport of lipids from high and low density lipoproteins via scavenger receptor‐BI. J Biol Chem 1999; 274: 32692–8
  • Ji Y., Jian B., Wang N., Sun Y., Moya M. L., Phillips M. C., et al. Scavenger receptor BI promotes high density lipoprotein‐mediated cellular cholesterol efflux. J Biol Chem 1997; 272: 20982–5
  • Gu X., Kozarsky K., Krieger M. Scavenger receptor class B, type I‐mediated [3H]cholesterol efflux to high and low density lipoproteins is dependent on lipoprotein binding to the receptor. J Biol Chem 2000; 275: 29993–30001
  • Liu T., Krieger M., Kan H. Y., Zannis V. I. The effects of mutations in helices 4 and 6 of apoA‐I on scavenger receptor class B type I (SR‐BI)‐mediated cholesterol efflux suggest that formation of a productive complex between reconstituted high density lipoprotein and SR‐BI is required for efficient lipid transport. J Biol Chem 2002; 277: 21576–84
  • Krieger M. Scavenger receptor class B type I is a multiligand HDL receptor that influences diverse physiologic systems. J Clin Invest 2001; 108: 793–7
  • Wang N., Lan D., Chen W., Matsuura F., Tall A. R. ATP‐binding cassette transporters G1 and G4 mediate cellular cholesterol efflux to high‐density lipoproteins. Proc Natl Acad Sci U S A 2004; 101: 9774–9
  • Zannis V. I., Cole F. S., Jackson C. L., Kurnit D. M., Karathanasis S. K. Distribution of apolipoprotein A‐I, C‐II, C‐III, and E mRNA in fetal human tissues. Time‐dependent induction of apolipoprotein E mRNA by cultures of human monocyte‐macrophages. Biochemistry 1985; 24: 4450–5
  • Chroni A., Liu T., Gorshkova I., Kan H. Y., Uehara Y., von Eckardstein A., et al. The central helices of apoA‐I can promote ATP‐binding cassette transporter A1 (ABCA1)‐mediated lipid efflux. Amino acid residues 220–231 of the wild‐type apoA‐I are required for lipid efflux in vitro and high density lipoprotein formation in vivo. J Biol Chem 2003; 278: 6719–30
  • Chroni A., Kan H. Y., Kypreos K. E., Gorshkova I. N., Shkodrani A., Zannis V. I. Substitutions of glutamate 110 and 111 in the middle helix 4 of human apolipoprotein A‐I (apoA‐I) by alanine affect the structure and in vitro functions of apoA‐I and induce severe hypertriglyceridemia in apoA‐I‐deficient mice. Biochemistry 2004; 43: 10442–57
  • Chroni A., Kan H. Y., Shkodrani A., Liu T., Zannis V. I. Deletions of Helices 2 and 3 of Human ApoA‐I Are Associated with Severe Dyslipidemia following Adenovirus‐Mediated Gene Transfer in ApoA‐I‐Deficient Mice. Biochemistry 2005; 44: 4108–17
  • Chroni A., Duka A., Kan H. Y., Liu T., Zannis V. I. Point mutations in apolipoprotein A‐I mimic the phenotype observed in patients with classical lecithin:cholesterol acyltransferase deficiency. Biochemistry 2005; 44: 14353–66
  • Chroni A., Koukos G., Duka A., Zannis V. I. The Carboxy‐Terminal Region of apoA‐I Is Required for the ABCA1‐Dependent Formation of alpha‐HDL But Not Prebeta‐HDL Particles in Vivo. Biochemistry 2007; 46: 5697–708
  • Koukos G., Chroni A., Duka A., Kardassis D., Zannis V. I. Naturally occurring and bioengineered apoA‐I mutations that inhibit the conversion of discoidal to spherical HDL: The abnormal HDL phenotypes can be corrected by treatment with LCAT. Biochem J 2007; 406: 167–74
  • Kypreos K. E., Zannis V. I. Pathway of biogenesis of apolipoprotein E‐containing HDL in vivo with the participation of ABCA1 and LCAT. Biochem J 2007; 403: 359–67
  • Kypreos K. E., Van Dijk K. W., Havekes L. M., Zannis V. I. Generation of a recombinant apolipoprotein E variant with improved biological functions: hydrophobic residues (LEU‐261, TRP‐264, PHE‐265, LEU‐268, VAL‐269) of apoE can account for the apoE‐induced hypertriglyceridemia. J Biol Chem 2005; 280: 6276–84
  • Drosatos K., Kypreos K. E., Zannis V. I. Residues Leu261, Trp264, and Phe265 account for apolipoprotein E‐induced dyslipidemia and affect the formation of apolipoprotein E‐containing high‐density lipoprotein. Biochemistry 2007; 46: 9645–53
  • Chroni A., Liu T., Fitzgerald M. L., Freeman M. W., Zannis V. I. Cross‐linking and lipid efflux properties of apoA‐I mutants suggest direct association between apoA‐I helices and ABCA1. Biochemistry 2004; 43: 2126–39
  • Nieland T. J., Chroni A., Fitzgerald M. L., Maliga Z., Zannis V. I., Kirchhausen T., et al. Cross‐inhibition of SR‐BI‐ and ABCA1‐mediated cholesterol transport by the small molecules BLT‐4 and glyburide. J Lipid Res 2004; 45: 1256–65
  • Chambenoit O., Hamon Y., Marguet D., Rigneault H., Rosseneu M., Chimini G. Specific docking of apolipoprotein A‐I at the cell surface requires a functional ABCA1 transporter. J Biol Chem 2001; 276: 9955–60
  • Reardon C. A., Kan H. Y., Cabana V., Blachowicz L., Lukens J. R., Wu Q., et al. In vivo studies of HDL assembly and metabolism using adenovirus‐mediated transfer of ApoA‐I mutants in ApoA‐I‐deficient mice. Biochemistry 2001; 40: 13670–80
  • Fitzgerald M. L., Morris A. L., Chroni A., Mendez A. J., Zannis V. I., Freeman M. W. ABCA1 and amphipathic apolipoproteins form high‐affinity molecular complexes required for cholesterol efflux. J Lipid Res 2004; 45: 287–94
  • Miccoli R., Bertolotto A., Navalesi R., Odoguardi L., Boni A., Wessling J., et al. Compound heterozygosity for a structural apolipoprotein A‐I variant, apo A‐I(L141R)Pisa, and an apolipoprotein A‐I null allele in patients with absence of HDL cholesterol, corneal opacifications, and coronary heart disease. Circulation 1996; 94: 1622–8
  • Miccoli R., Zhu Y., Daum U., Wessling J., Huang Y., Navalesi R., et al. A natural apolipoprotein A‐I variant, apoA‐I (L141R)Pisa, interferes with the formation of alpha‐high density lipoproteins (HDL) but not with the formation of pre beta 1‐HDL and influences efflux of cholesterol into plasma. J Lipid Res 1997; 38: 1242
  • Pisciotta L., Miccoli R., Cantafora A., Calabresi L., Tarugi P., Alessandrini P., et al. Recurrent mutations of the apolipoprotein A‐I gene in three kindreds with severe HDL deficiency. Atherosclerosis 2003; 167: 335–45
  • Navalesi R., Miccoli R., Odoguardi L., Funke H., von Eckardstein A., Wiebusch H., et al. Genetically determined absence of HDL‐cholesterol and coronary atherosclerosis. Lancet 1995; 346: 708–9
  • Gylling H., Relas H., Miettinen H. E., Radhakrishnan R., Miettinen T. A. Delayed postprandial retinyl palmitate and squalene removal in a patient heterozygous for apolipoprotein A‐IFIN mutation (Leu 159–>Arg) and low HDL cholesterol level without coronary artery disease. Atherosclerosis 1996; 127: 239–43
  • Miettinen H. E., Gylling H., Miettinen T. A., Viikari J., Paulin L., Kontula K. Apolipoprotein A‐IFin. Dominantly inherited hypoalphalipoproteinemia due to a single base substitution in the apolipoprotein A‐I gene. Arterioscler Thromb Vasc Biol 1997; 17: 83–90
  • Miettinen H. E., Jauhiainen M., Gylling H., Ehnholm S., Palomaki A., Miettinen T. A., et al. Apolipoprotein A‐IFIN (Leu159–>Arg) mutation affects lecithin cholesterol acyltransferase activation and subclass distribution of HDL but not cholesterol efflux from fibroblasts. Arterioscler Thromb Vasc Biol 1997; 17: 3021–32
  • Daum U., Langer C., Duverger N., Emmanuel F., Benoit P., Denefle P., et al. Apolipoprotein A‐I (R151C)Paris is defective in activation of lecithin: cholesterol acyltransferase but not in initial lipid binding, formation of reconstituted lipoproteins, or promotion of cholesterol efflux. J Mol Med 1999; 77: 614–22
  • Bruckert E., von Eckardstein A., Funke H., Beucler I., Wiebusch H., Turpin G., et al. The replacement of arginine by cysteine at residue 151 in apolipoprotein A‐I produces a phenotype similar to that of apolipoprotein A‐IMilano. Atherosclerosis 1997; 128: 121–8
  • Leren T. P., Bakken K. S., Daum U., Ose L., Berg K., Assmann G., et al. Heterozygosity for apolipoprotein A‐I(R160L)Oslo is associated with low levels of high density lipoprotein cholesterol and HDL‐subclass LpA‐I/A‐ II but normal levels of HDL‐subclass LpA‐I. J Lipid Res 1997; 38: 121–31
  • Roosbeek S., Vanloo B., Duverger N., Caster H., Breyne J., De Beun I., et al. Three arginine residues in apolipoprotein A‐I are critical for activation of lecithin:cholesterol acyltransferase. J Lipid Res 2001; 42: 31–40
  • Koukos G., Chroni A., Duka A., Kardassis D., Zannis V. I. Lecithin:Cholesterol Acyl Transferase Can Rescue the Abnormal Phenotype Produced by the Natural Apolipoprotein A‐I Mutations (Leu141Arg)Pisa and (Leu159Arg)FIN. Biochemistry 2007; 46: 10713–21
  • Huuskonen J., Olkkonen V. M., Jauhiainen M., Ehnholm C. The impact of phospholipid transfer protein (PLTP) on HDL metabolism. Atherosclerosis 2001; 155: 269–81
  • Pussinen P. J., Jauhiainen M., Metso J., Pyle L. E., Marcel Y. L., Fidge N. H., et al. Binding of phospholipid transfer protein (PLTP) to apolipoproteins A‐I and A‐II: location of a PLTP binding domain in the amino terminal region of apoA‐I. J Lipid Res 1998; 39: 152–61
  • Yuhanna I. S., Zhu Y., Cox B. E., Hahner L. D., Osborne‐Lawrence S., Lu P., et al. High‐density lipoprotein binding to scavenger receptor‐BI activates endothelial nitric oxide synthase. Nat Med 2001; 7: 853–7
  • Rader D. J. High‐density lipoproteins and atherosclerosis. Am J Cardiol 2002; 90: 62i–70i
  • Navab M., Hama S. Y., Anantharamaiah G. M., Hassan K., Hough G. P., Watson A. D., et al. Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: steps 2 and 3. J Lipid Res 2000; 41: 1495–508
  • Mineo C., Yuhanna I. S., Quon M. J., Shaul P. W. High density lipoprotein‐induced endothelial nitric‐oxide synthase activation is mediated by Akt and MAP kinases. J Biol Chem 2003; 278: 9142–9
  • Li X., Kypreos K., Zanni E. E., Zannis V. Domains of apoE required for binding to apoE receptor 2 and to phospholipids: Implications for the functions of apoE in the brain. Biochemistry 2003; 42: 10406–17
  • Boyles J. K., Pitas R. E., Wilson E., Mahley R. W., Taylor J. M. Apolipoprotein E associated with astrocytic glia of the central nervous system and with nonmyelinating glia of the peripheral nervous system. J Clin Invest 1985; 76: 1501–13
  • Chroni A., Nieland T. J., Kypreos K. E., Krieger M., Zannis V. I. SR‐BI mediates cholesterol efflux via its interactions with lipid‐bound ApoE. Structural mutations in SR‐BI diminish cholesterol efflux. Biochemistry 2005; 44: 13132–43
  • Cao D., Fukuchi K., Wan H., Kim H., Li L. Lack of LDL receptor aggravates learning deficits and amyloid deposits in Alzheimer transgenic mice. Neurobiol Aging 2006; 27: 1632–43
  • DeMattos R. B., Cirrito J. R., Parsadanian M., May P. C., O'Dell M. A., Taylor J. W., et al. ApoE and clusterin cooperatively suppress Abeta levels and deposition: evidence that ApoE regulates extracellular Abeta metabolism in vivo. Neuron 2004; 41: 193–202
  • Tanzi R. E., Moir R. D., Wagner S. L. Clearance of Alzheimer's Abeta peptide: the many roads to perdition. Neuron 2004; 43: 605–8
  • Shibata M., Yamada S., Kumar S. R., Calero M., Bading J., Frangione B., et al. Clearance of Alzheimer's amyloid‐ss(1–40) peptide from brain by LDL receptor‐related protein‐1 at the blood‐brain barrier. J Clin Invest 2000; 106: 1489–99
  • Deane R., Wu Z., Sagare A., Davis J., Du Y. S., Hamm K., et al. LRP/amyloid beta‐peptide interaction mediates differential brain efflux of Abeta isoforms. Neuron 2004; 43: 333–44
  • Zerbinatti C. V., Bu G. LRP and Alzheimer's disease. Rev Neurosci 2005; 16: 123–35
  • Van Uden E., Mallory M., Veinbergs I., Alford M., Rockenstein E., Masliah E. Increased extracellular amyloid deposition and neurodegeneration in human amyloid precursor protein transgenic mice deficient in receptor‐associated protein. J Neurosci 2002; 22: 9298–304
  • Ruiz J., Kouiavskaia D., Migliorini M., Robinson S., Saenko E. L., Gorlatova N., et al. The apoE isoform binding properties of the VLDL receptor reveal marked differences from LRP and the LDL receptor. J Lipid Res 2005; 46: 1721–31
  • Bales K. R., Verina T., Cummins D. J., Du Y., Dodel R. C., Saura J., et al. Apolipoprotein E is essential for amyloid deposition in the APP(V717F) transgenic mouse model of Alzheimer's disease. Proc Natl Acad Sci U S A 1999; 96: 15233–8
  • Burns M. P., Noble W. J., Olm V., Gaynor K., Casey E., LaFrancois J., et al. Co‐localization of cholesterol, apolipoprotein E and fibrillar Abeta in amyloid plaques. Brain Res Mol Brain Res 2003; 110: 119–25
  • Miao J., Vitek M. P., Xu F., Previti M. L., Davis J., Van Nostrand W. E. Reducing cerebral microvascular amyloid‐beta protein deposition diminishes regional neuroinflammation in vasculotropic mutant amyloid precursor protein transgenic mice. J Neurosci 2005; 25: 6271–7
  • Ajees A. A., Anantharamaiah G. M., Mishra V. K., Hussain M. M., Murthy H. M. Crystal structure of human apolipoprotein A‐I: insights into its protective effect against cardiovascular diseases. Proc Natl Acad Sci U S A 2006; 103: 2126–31
  • Scott B. R., McManus D. C., Franklin V., McKenzie A. G., Neville T., Sparks D. L., et al. The N‐terminal globular domain and the first class A amphipathic helix of apolipoprotein A‐I are important for lecithin:cholesterol acyltransferase activation and the maturation of high density lipoprotein in vivo. J Biol Chem 2001; 276: 48716–24
  • Sorci‐Thomas M. G., Thomas M., Curtiss L., Landrum M. Single repeat deletion in ApoA‐I blocks cholesterol esterification and results in rapid catabolism of delta6 and wild‐type ApoA‐I in transgenic mice. J Biol Chem 2000; 275: 12156–63

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