Macrophage paraoxonase 2 (PON2) expression is upregulated by unesterified cholesterol through activation of the phosphatidylinositol 3-kinase (PI 3K) pathway

Biological Chemistry

Volumn 388, Issue 12, 2007, Pages 1353-1358

  Shiner, Maayan ^a   Fuhrman, Bianca ^a   Aviram, Michael ^a  

^a RAMBAM MEDICAL CENTER   (Israel)

Author keywords

Macrophages; Paraoxonase 2; PI3K; Unesterified cholesterol

Indexed keywords

2 MORPHOLINO 8 PHENYLCHROMONE; ARYLDIALKYLPHOSPHATASE; ARYLDIALKYLPHOSPHATASE 2; CHOLESTEROL; CHOLESTEROL ACYLTRANSFERASE INHIBITOR; CHOLESTEROL ESTER; LOW DENSITY LIPOPROTEIN; PHOSPHATIDYLINOSITOL 3 KINASE; UNCLASSIFIED DRUG; WORTMANNIN;

ACETYLATION; ARTICLE; CONTROLLED STUDY; ENZYME ACTIVATION; HUMAN; HUMAN CELL; INCUBATION TIME; MACROPHAGE; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; UPREGULATION;

1-PHOSPHATIDYLINOSITOL 3-KINASE; ANIMALS; ARYLDIALKYLPHOSPHATASE; BLOTTING, WESTERN; CHOLESTEROL; CHOLESTEROL, LDL; ENZYME ACTIVATION; HUMANS; INDICATORS AND REAGENTS; MACROPHAGES; MICE; MICROSCOPY, CONFOCAL; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; SIGNAL TRANSDUCTION; UP-REGULATION;

EID: 36248962838     PISSN: 14316730     EISSN: 14374315     Source Type: Journal    
DOI: 10.1515/BC.2007.145     Document Type: Article

References (27)

1. Aviram, M. (1983). Plasma lipoprotein separation by discontinuous density gradient ultracentrifugation in hyperlipoproteinemic patients. Biochem. Med. 30, 111-118.
2. Aviram, M. and Rosenblat, M. (2004). Paraoxonases 1, 2, and 3, oxidative stress, and macrophage foam cell formation during atherosclerosis development. Free Radic. Biol. Med. 37, 1304-1316.
3. Aviram, M. and Rosenblat, M. (2005). Paraoxonases and cardiovascular diseases: pharmacological and nutritional influences. Curr. Opin. Lipidol. 16, 393-399.
4. Cathcart, M.K. (2004). Regulation of superoxide anion production by NADPH oxidase in monocytes/macrophages: contributions to atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 24, 23-28.
5. Devries-Seimon, T., Li, Y., Yao, P.M., Stone, E., Wang, Y., Davis, R.J., Flavell, R., and Tabas, I. (2005). Cholesterol-induced macrophage apoptosis requires ER stress pathways and engagement of the type A scavenger receptor. J. Cell. Biol. 171, 61-73.
6. Fazio, S., Major, A.S., Swift, L.L., Gleaves, L.A., Accad, M., Linton, M.F. and Farese, R.V. (2001). Increased atherosclerosis in LDL receptor-null mice lacking ACAT1 in macrophages. J. Clin. Invest. 107, 163-171.
7. Feng, B., Yao, P.M., Li, Y., Devlin, C.M., Zhang, D., Harding, H.P., Sweeney, M., Rong, J.X., Kuriakose, G., Fisher, E.A., et al. (2003). The endoplasmic reticulum is the site of cholesterolinduced cytotoxicity in macrophages. Nat. Cell Biol. 5, 781-792.
8. Frey, R.S., Gao, X., Javaid, K., Siddiqui, S.S., Rahman, A., and Malik, A.B. (2006). Phosphatidylinositol 3-kinase gamma signaling through protein kinase Cζ induces NADPH oxidase-mediated oxidant generation and NF-κB activation in endothelial cells. J. Biol. Chem. 281, 16128-16138.
9. Goldstein, J.L. and Brown, M.S. (1977). Atherosclerosis: the low-density lipoprotein receptor hypothesis. Metabolism 26, 1257-1275.
10. Harding, H.P., Calfon, M., Urano, F., Novoa, I., and Ron, D. (2002). Transcriptional and translational control in the mammalian unfolded protein response. Annu. Rev. Cell Dev. Biol. 18, 575-599.
11. Hawkins, P.T., Davidson, K., and Stephens, L.R. (2007). The role of PI3Ks in the regulation of the neutrophil NADPH oxidase. Biochem. Soc. Symp. 74, 59-67.
12. Horke, S., Witte, I., Wilgenbus, P., Kruger, M., Strand, D., and Forstermann, U. (2007). Paraoxonase-2 reduced oxidative stress in vascular cells and decreases endoplasmic reticulum stress-induced caspase activation. Circulation 115, 2055-2064.
13. Iaccio, A., Collinet, C., Gesualdi, N.M., and Ammendola, R. (2007). Protein kinase C-alpha and -delta are required for NADPH oxidase activation in WKYMVm-stimulated IMR90 human fibroblasts. Arch. Biochem. Biophys. 459, 288-294.
14. Knight, B.L., Patel, D.D., and Soutar, A.K. (1983). The regulation of 3-hydroxy-3-methylglutaryl-CoA reductase activity, cholesterol esterification and the expression of low-density lipoprotein receptors in cultured monocyte-derived macrophages. Biochem. J. 210, 523-532.
15. Lusis, A.J. (2000). Atherosclerosis. Nature 404, 233-241.
16. Ng, C.J., Wadleigh, D.J., Gangopadhyay, A., Hama, S., Grijalva, V.R., Navab, M., Fogelman, A.M., and Reddy, S.T. (2001). Paraoxonase-2 is a ubiquitously expressed protein with antioxidant properties and is capable of preventing cell-mediated oxidative modification of low density lipoprotein. J. Biol. Chem. 276, 44444-44449.
17. Patil, C. and Walter, P. (2001). Intracellular signaling from the endoplasmic reticulum to the nucleus: the unfolded protein response in yeast and mammals. Curr. Opin. Cell Biol. 13, 349-355.
18. Rosenblat, M., Draganov, D., Watson, C.E., Bisgaier, C.L., La Du, B.N., and Aviram, M. (2003). Mouse macrophage paraoxonase 2 activity is increased whereas cellular paraoxonase 3 activity is decreased under oxidative stress. Arterioscler. Thromb. Vasc. Biol. 23, 468-474.
19. Rosenblat, M., Hayek, T., Hussein, K., and Aviram, M. (2004). Decreased macrophage paraoxonase 2 expression in patients with hypercholesterolemia is the result of their increased cellular cholesterol content: effect of atorvastatin therapy. Arterioscler. Thromb. Vasc. Biol. 24, 175-180.
20. Schroder, M. and Kaufman, R.J. (2005). ER stress and the unfolded protein response. Mutat. Res. 569, 29-63.
21. Shiner, M., Fuhrman, B., and Aviram, M. (2004). Paraoxonase 2 (PON2) expression is upregulated via a reduced-nicotinamide-adenine-dinucleotide- phosphate (NADPH)-oxidase-dependent mechanism during monocytes differentiation into macrophages. Free Radic. Biol. Med. 37, 2052-2063.
22. Shiner, M., Fuhrman, B., and Aviram, M. (2006). A biphasic Ushape effect of cellular oxidative stress on the macrophage anti-oxidant paraoxonase 2 (PON2) enzymatic activity. Biochem. Biophys. Res. Commun. 349, 1094-1099.
23. Shiner, M., Fuhrman, B., and Aviram, M. (2007). Macrophage paraoxonase 2 (PON2) expression is up-regulated by pomegranate juice phenolic anti-oxidants via PPARγ and AP-1 pathway activation. Atherosclerosis, in press.
24. Tabas, I. (2002). Consequences of cellular cholesterol accumulation: basic concepts and physiological implications. J. Clin. Invest. 110, 905-911.
25. Urbani, L. and Simoni, R.D. (1990). Cholesterol and vesicular stomatitis virus G protein take separate routes from the endoplasmic reticulum to the plasma membrane. J. Biol. Chem. 265, 1919-1923.
26. Yao, P.M. and Tabas, I. (2001). Free cholesterol loading of macrophages is associated with widespread mitochondrial dysfunction and activation of the mitochondrial apoptosis pathway. J. Biol. Chem. 276, 42468-42476.
27. Zhou, J., Chew, M., Ravn, H.B., and Falk, E. (1999). Plaque pathology and coronary thrombosis in the pathogenesis of acute coronary syndromes. Scand. J. Clin. Lab. Invest. (Suppl.) 230, 3-11.