Atorvastatin Inhibits CD68 Expression in Aortic Root Through a GRP78-Involved Pathway

Cardiovascular Drugs and Therapy

Volumn 28, Issue 6, 2014, Pages 523-532

  Li, Ling ^a   Wang, Yu ^a   Xu, Yan ^a   Chen, Lianfeng ^a   Fang, Quan ^a   Yan, Xiaowei ^a  

^a PEKING UNION MEDICAL COLLEGE HOSPITAL   (China)

Author keywords

Atherosclerosis; Atorvastatin; CD68; Diabetes mellitus; ER stress; GRP78

Indexed keywords

ATORVASTATIN; CD68 ANTIGEN; COMPLEMENTARY DNA; GLUCOSE; GLUCOSE REGULATED PROTEIN 78; HIGH DENSITY LIPOPROTEIN CHOLESTEROL; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR; LOW DENSITY LIPOPROTEIN CHOLESTEROL; RNA; TRIACYLGLYCEROL; VOMITOXIN; CD68 ANTIGEN, HUMAN; DIFFERENTIATION ANTIGEN; HEAT SHOCK PROTEIN; HEPTANOIC ACID DERIVATIVE; HYPOCHOLESTEROLEMIC AGENT; LEUKOCYTE ANTIGEN; MOLECULAR CHAPERONE GRP78; PYRROLE DERIVATIVE; TRICHOTHECENE DERIVATIVE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIGEN EXPRESSION; AORTA ROOT; ARTICLE; ATHEROSCLEROSIS; BODY WEIGHT; CONTROLLED STUDY; DIABETES MELLITUS; DRUG DOSE COMPARISON; DRUG MEGADOSE; ENDOPLASMIC RETICULUM; ENDOPLASMIC RETICULUM STRESS; GLUCOSE BLOOD LEVEL; IMMUNOHISTOCHEMISTRY; IN VITRO STUDY; IN VIVO STUDY; LIPID BLOOD LEVEL; LIPOGENESIS; LOW DRUG DOSE; MACROPHAGE; MALE; NONHUMAN; PROTEIN EXPRESSION; RANDOMIZED CONTROLLED TRIAL; REAL TIME POLYMERASE CHAIN REACTION; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; STREPTOZOTOCIN-INDUCED DIABETES MELLITUS; SYRIAN HAMSTER; WESTERN BLOTTING; ANIMAL; AORTA; DRUG EFFECTS; MESOCRICETUS; METABOLISM; SIGNAL TRANSDUCTION;

ANIMALS; ANTICHOLESTEREMIC AGENTS; ANTIGENS, CD; ANTIGENS, DIFFERENTIATION, MYELOMONOCYTIC; AORTA; ATHEROSCLEROSIS; GLUCOSE; HEAT-SHOCK PROTEINS; HEPTANOIC ACIDS; MACROPHAGES; MALE; MESOCRICETUS; PYRROLES; SIGNAL TRANSDUCTION; TRICHOTHECENES;

EID: 84916242036     PISSN: 09203206     EISSN: 15737241     Source Type: Journal    
DOI: 10.1007/s10557-014-6556-3     Document Type: Article

References (35)

1. Stoger JL, Gijbels MJ, van der Velden S, Manca M, van der Loos CM, Biessen EA, et al. Distribution of macrophage polarization markers in human atherosclerosis. Atherosclerosis. 2012;225(2):461–8.
2. Zhang C, Zheng H, Yu Q, Yang P, Li Y, Cheng F, et al. A practical method for quantifying atherosclerotic lesions in rabbits. J Comp Pathol. 2010;142(2–3):122–8.
3. Figueroa AL, Subramanian SS, Cury RC, Truong QA, Gardecki JA, Tearney GJ, et al. Distribution of inflammation within carotid atherosclerotic plaques with high-risk morphological features: a comparison between positron emission tomography activity, plaque morphology, and histopathology. Circ Cardiovasc Imaging. 2012;5(1):69–77.
4. Dickhout JG, Sood SK, Austin RC. Role of endoplasmic reticulum calcium disequilibria in the mechanism of homocysteine-induced ER stress. Antioxid Redox Signal. 2007;9(11):1863–73.
5. Minamino T, Kitakaze M. ER stress in cardiovascular disease. J Mol Cell Cardiol. 2010;48(6):1105–10.
6. Korennykh A, Walter P. Structural basis of the unfolded protein response. Annu Rev Cell Dev Biol. 2012;28:251–77.
7. Ni M, Lee AS. ER chaperones in mammalian development and human diseases. FEBS Lett. 2007;581(19):3641–51.
8. Misra UK, Pizzo SV. Upregulation of GRP78 and antiapoptotic signaling in murine peritoneal macrophages exposed to insulin. J Leukoc Biol. 2005;78(1):187–94.
9. Chen JC, Wu ML, Huang KC, Lin WW. HMG-CoA reductase inhibitors activate the unfolded protein response and induce cytoprotective GRP78 expression. Cardiovasc Res. 2008;80(1):138–50.
10. Feaver RE, Hastings NE, Pryor A, Blackman BR. GRP78 upregulation by atheroprone shear stress via p38-, alpha2beta1-dependent mechanism in endothelial cells. Arterioscler Thromb Vasc Biol. 2008;28(8):1534–41.
11. Hagenaars T, Gussenhoven EJ, Poldermans D, van Urk H, van der Lugt A. Rationale and design for the SARIS trial; effect of statin on atherosclerosis and vascular remodeling assessed with intravascular sonography. Cardiovasc Drug Ther. 2001;15(4):339–43.
12. Thomas MK, Narang D, Lakshmy R, Gupta R, Naik N, Maulik SK. Correlation between inflammation and oxidative stress in normocholesterolemic coronary artery disease patients ‘on’ and ‘off’ atorvastatin for short time intervals. Cardiovasc Drug Ther. 2006;20(1):37–44.
13. Simsek S, Schalkwijk CG, Wolffenbuttel BH. Effects of rosuvastatin and atorvastatin on glycaemic control in type 2 diabetes–-the CORALL study. Diabet Med. 2012;29(5):628–31.
14. Llaverias G, Noe V, Penuelas S, Vazquez-Carrera M, Sanchez RM, Laguna JC, et al. Atorvastatin reduces CD68, FABP4, and HBP expression in oxLDL-treated human macrophages. Biochem Biophys Res Commun. 2004;318(1):265–74.
15. Zhang W, Liu M, Wu Y, Zhu P, Yin C, Zhang W, et al. Protective effects of atorvastatin on chronic allograft nephropathy in rats. J Surg Res. 2007;143(2):428–36.
16. Wilson RD, Islam MS. Fructose-fed streptozocin-injected rat: an alternative model for type 2 diabetes. Pharmacol Rep. 2012;64(1):129–39.
17. Zhang M, Lv XY, Li J, Xu ZG, Cheng L. The characterization of high-fat diet and multiple low-dose streptozotocin induced type 2 diabetes rat model. Exp Diabetes Res. 2008;2008:704045.
18. Wang CJ, Zhou ZG. Survivin expression quantified by Image Pro-Plus compared with visual assessment. Appl Immunohistochem Mol Morphol. 2009;17(6):530–5.
19. Yang GH, Li S, Pestka JJ. Downregulation of the endoplasmic reticulum chaperone GRP78/BiP by vomitoxin (Deoxynivalenol). Toxicol Appl Pharmacol. 2000;162(3):207–17.
20. Lin CS, Lin FY, Ho LJ, Tsai CS, Cheng SM, Wu WL, et al. PKCδ signalling regulates SR-A and CD36 expression and foam cell formation. Cardiovasc Res. 2012;95(3):346–55.
21. Feig JE, Parathath S, Rong JX, Mick SL, Vengrenyuk Y, Grauer L, et al. Reversal of hyperlipidemia with a genetic switch favorably affects the content and inflammatory state of macrophages in atherosclerotic plaques. Circulation. 2011;123(9):989–98.
22. Feig JE, Shang Y, Rotllan N, Vengrenyuk Y, Wu C, Shamir R, et al. Statins promote the regression of atherosclerosis via activation of the CCR7-dependent emigration pathway in macrophages. PLoS One. 2011;6(12):e28534.
23. Inagi R. Inhibitors of advanced glycation and endoplasmic reticulum stress. Methods Enzymol. 2011;491:361–80.
24. Pineau L, Colas J, Dupont S, Beney L, Fleurat-Lessard P, Berjeaud JM, et al. Lipid-induced ER stress: synergistic effects of sterols and saturated fatty acids. Traffic. 2009;10(6):673–90.
25. Booth L, Cazanave SC, Hamed HA, Yacoub A, Ogretmen B, Chen CS, et al. OSU-03012 suppresses GRP78/BiP expression that causes PERK-dependent increases in tumor cell killing. Cancer Biol Ther. 2012;13(4):224–36.
26. Quinones QJ, de Ridder GG, Pizzo SV. GRP78: a chaperone with diverse roles beyond the endoplasmic reticulum. Histol Histopathol. 2008;23(11):1409–16.
27. Kurokawa M, Hideshima M, Ishii Y, Kyuwa S, Yoshikawa Y. Aortic ER stress in streptozotocin-induced diabetes mellitus in APA hamsters. Exp Anim. 2009;58(2):113–21.
28. Huang LW, Lin CY, Lee CC, Liu TZ, Jeng CJ. Overexpression of GRP78 is associated with malignant transformation in epithelial ovarian tumors. Appl Immunohistochem Mol Morphol. 2012;20(4):381–5.
29. Song XJ, Yang CY, Liu B, Wei Q, Korkor MT, Liu JY, et al. Atorvastatin inhibits myocardial cell apoptosis in rat model with post-myocardial infarction heart failure by downregulating ER stress response. Int J Med Sci. 2011;8(7):564–72.
30. Jiang Y, Lv H, Liao M, Xu X, Huang S, Tan H, et al. GRP78 counteracts cell death and protein aggregation caused by mutant huntingtin proteins. Neurosci Lett. 2012;516(2):182–7.
31. Blanca M, Esther P, Teresa P. Glucose-regulated protein 78 and platelet deposition: effect of rosuvastatin. Arterioscler Thromb Vasc Biol. 2010;30(6):1246–52.
32. Shi Y, Porter K, Parameswaran N, Bae HK, Pestka JJ. Role of GRP78/BiP degradation and ER stress in deoxynivalenol-induced interleukin-6 upregulation in the macrophage. Toxicol Sci. 2009;109(2):247–55.
33. Chen L, Xu S, Liu L, Wen X, Xu Y, Chen J, et al. Cab45S inhibits the ER stress-induced IRE-JNK pathway and apoptosis via GRP78/Bip. Cell Death Dis. 2014;8(5):e1219.
34. Pestka JJ. Deoxynivalenol-induced proinflammatory gene expression: mechanisms and pathological sequelae. Toxins. 2010;2(6):1300–17.
35. Dickhout JG, Lhotak S, Hilditch BA, Basseri S, Colgan SM, Lynn EG, et al. Induction of the unfolded protein response after monocyte to macrophage differentiation augments cell survival in early atherosclerotic lesions. FASEB J. 2011;25(2):576–89.