Monocyte-specific Bcl-2 expression attenuates inflammation and heart failure in monocyte chemoattractant protein-1 (MCP-1)-induced cardiomyopathy

Cardiovascular Research

Volumn 71, Issue 1, 2006, Pages 139-148

  Niu, Jianli ^a   Azfer, Asim ^a   Kolattukudy, Pappachan E ^a  

^a Burnett School of Biomedical Sciences   (United States)

Author keywords

Apoptosis; Cardiomyopathy; Inflammation; Monocyte chemoattractant protein 1; Transgenic animal model

Indexed keywords

C REACTIVE PROTEIN; CYTOKINE; INTERLEUKIN 1BETA; INTERLEUKIN 6; MONOCYTE CHEMOTACTIC PROTEIN 1; PROTEIN BCL 2; TUMOR NECROSIS FACTOR ALPHA;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CARDIOMYOPATHY; CELL INFILTRATION; CONTROLLED STUDY; CROSS BREEDING; CYTOKINE PRODUCTION; DISEASE COURSE; HEART FAILURE; HEART FUNCTION; IN VIVO STUDY; INFLAMMATION; MACROPHAGE ACTIVATION; MALE; MONONUCLEAR CELL; MOUSE; MOUSE STRAIN; NONHUMAN; PRIORITY JOURNAL; PROTEIN BLOOD LEVEL; PROTEIN EXPRESSION; STATISTICAL SIGNIFICANCE; TRANSGENIC MOUSE; WILD TYPE;

ANIMALS; APOPTOSIS; BIOLOGICAL MARKERS; C-REACTIVE PROTEIN; CHEMOKINE CCL2; CHEMOTAXIS, LEUKOCYTE; ECHOCARDIOGRAPHY; GENE EXPRESSION; HEART FAILURE; HEART FAILURE, CONGESTIVE; IMMUNOHISTOCHEMISTRY; IN SITU NICK-END LABELING; INTERLEUKIN-1BETA; INTERLEUKIN-6; LYMPHOCYTES; MACROPHAGE ACTIVATION; MICE; MICE, MUTANT STRAINS; MICE, TRANSGENIC; MYOCARDIUM; PROTO-ONCOGENE PROTEINS C-BCL-2; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; SURVIVAL ANALYSIS; TUMOR NECROSIS FACTOR-ALPHA;

EID: 33744947775     PISSN: 00086363     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.cardiores.2006.03.008     Document Type: Article

References (38)

1. Ikeda U. Inflammation and coronary artery disease. Curr Vasc Pharmacol 1 (2003) 65-70
2. Nian M., Lee P., Khaper N., and Liu P. Inflammatory cytokines and postmyocardial infarction remodeling. Circ Res 94 (2004) 1543-1553
3. Hansson G.K. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 352 (2005) 1685-1695
4. Dawson J., Miltz W., Mir A.K., and Wiessner C. Targeting monocyte chemoattractant protein-1 signaling in disease. Expert Opin Ther Targets 7 (2003) 35-48
5. Sheikine Y., and Hansson G.K. Chemokines and atherosclerosis. Ann Med 36 (2004) 98-118
6. Hayashidani S., Tsutsui H., Shiomi T., Ikeuchi M., Matsusaka H., Suematsu N., et al. Anti-monocyte chemoattractant protein-1 gene therapy attenuates left ventricular remodeling and failure after experimental myocardial infarction. Circulation 108 (2003) 1-7
7. Aukrust P., Damäs J.K., Gullestad L., and Fröland S.S. Chemokines in myocardial failure-pathogenic importance and potential therapeutic targets. Clin Exp Immunol 124 (2001) 343-345
8. Becker L.C. Yin and Yang of MCP-1. Circ Res 96 (2005) 812-814
9. Kolattukudy P.E., Quach T., Bergese S., Breckenridge S., Hensley J., Altschuld R., et al. Myocarditis induced by targeted expression of the MCP-1 gene in murine cardiac muscle. Am J Pathol 152 (1998) 101-111
10. Moldovan N.I., Goldschmidt-Clermont P.J., Parker-Thornburg J., Shapiro S.D., and Kolattukudy P.E. Contribution of monocytes/macrophages to compensatory neovascularization: the drilling of metalloelastase-positive tunnels in ischemic myocardium. Circ Res 87 (2000) 378-384
11. Fadeel B., and Orrenius S. Apoptosis: a basic biological phenomenon with wide-ranging implications in human disease. J Intern Med 258 (2005) 479-517
12. Kang P.M., and Izumo S. Apoptosis and heart failure: a critical review of the literature. Circ Res 86 (2000) 1107-1113
13. Foo R.S., Mani K., and Kitsis R.N. Death begets failure in the heart. J Clin Invest 115 (2005) 565-571
14. Takemura G., Ohno M., Hayakawa Y., Misao J., Kanoh M., Ohno A., et al. Role of apoptosis in the disappearance of infiltrated and proliferated interstitial cells after myocardial infarction. Circ Res 82 (1998) 1130-1138
15. Ikeda S., Hamada M., and Hiwada K. Contribution of non-cardiomyocyte apoptosis to cardiac remodeling that occurs in the transition from compensated hypertrophy to heart failure in spontaneously hypertensive rats. Clin Sci 97 (1999) 239-246
16. Seko Y., Kayagaki N., Seino K.I., Yagita H., Okumura K., and Nagai R. Role of Fas/FasL pathway in the activation of infiltrating cells in murine acute myocarditis caused by coxsackievirus B3. J Am Coll Cardiol 39 (2002) 1399-1403
17. Maderna P., and Godson C. Phagocytosis of apoptotic cells and the resolution of inflammation. Biochim Biophys Acta 1639 (2003) 141-151
18. Hanayama R., Tanaka M., Miyasaka K., Aozasa K., Koike M., Uchiyama Y., et al. Autoimmune disease and impaired uptake of apoptotic cells in MFG-E8-dificient mice. Science 304 (2004) 1147-1150
19. Lagasse E., and Weissman I.L. Enforced expression of Bcl-2 in monocytes rescue macrophages and partially reverses osteopetrosis in op/op mice. Cell 89 (1997) 1021-1031
20. Muller P.Y., Janovjak H., Miserez A.R., and Dobbie Z. Processing of gene expression data generated by quantitative real-time RT-PCR. Biotechniques 32 (2002) 1372-1379
21. Brown S.B., and Savill J. Phagocytosis triggers macrophage release of Fas ligand and induces apoptosis of bystander leukocytes. J Immunol 162 (1999) 2110-2119
22. Stuart L.M., Savill J., and Lacy-Hulbert A. Apoptotic cells and innate immune stimuli combine to regulate macrophage cytokine secretion. J Immunol 171 (2003) 2610-2615
23. Lecnen P.J., De Bruijn M.F., Voerman J.S., Campbell P.A., and Van Ewijk W. Markers of mouse macrophage development detected by monoclonal antibodies. J Immunol Methods 174 (1994) 5-10
24. Yeh E.T., and Willerson J.T. Coming of age C-reactive protein: using inflammation markers in cardiology. Circulation 107 (2003) 730-732
25. Kroemer G. The proto-oncogene Bcl-2 and its role in regulating apoptosis. Nat Med 3 (1997) 614-620
26. Misao J., Hayakawa Y., Ohno M., Kato S., Fujiwara T., and Fujiwara H. Expression of Bcl-2 protein, an inhibitor of apoptosis, and bax, an accelerator of apoptosis, in ventricular myocytes of humans with myocardial infarction. Circulation 94 (1996) 1506-1512
27. Imanishi T., Han D.K.M., Hofstra L., Hano T., Nishio I., Liles W.C., et al. Apoptosis of vascular smooth muscle cells is induced by Fas ligand derived from monocytes/macrophages. Atherosclerosis 161 (2002) 143-151
28. Lee P., Sata M., Lefer D.J., Factor S.M., Walsh K., and Kitsis R.N. Fas pathway is a critical mediator for cardiac myocyte death and MI during ischemia-reperfusion in vivo. Am J Physiol Heart Circ Physiol 184 (2003) H456-H463
29. O'Connel J. Role of Fas-FasL in inflammatory disease. Expert Rev Mol Med 10 (2001) 1-18
30. Andreotti F., Porto I., Crea F., and Maseri A. Inflammation gene polymorphisms and ischemic heart disease: review of population association studies. Heart 87 (2002) 107-112
31. Anderson L. Candidate-based proteomics in the search for biomarkers of cardiovascular disease. J Physiol 563 (2005) 23-60
32. Niu J., Azfer A., Deucher M.F., Goldschmidt-Clermont P.J., and Kolattukudy P.E. Targeted myocardial expression of soluble Fas prevents the development of heart failure in mice with cardiac-specific expression of monocyte chemoattractant protein-1. Circulation 110 Suppl. III (2004) III-30 [Abstract]
33. Han K.H., Hong K.H., Park J.H., Ko J., Kang D.H., Choi K.J., et al. C-reactive protein promotes monocyte chemoattractant protein-1-mediated chemotaxis through upregulation CC chemokine receptor 2 expression in human monocytes. Circulation 109 (2004) 2566-2571
34. L serve an anti-inflammatory function in endothelial cells through inhibition of NF-kB. J Clin Invest 103 (1999) 543-553
35. Sun Z., and Andersson R. NF-kappaB activation and inhibition: a review. Shock 18 (2002) 99-106
36. Lakics V., Medvedev A.E., Okada S., and Vogel S.N. Inhibition of LPS-induced cytokines by BCL-xl in a murine macrophage cell line. J Immunol 165 (2000) 2729-2737
37. Wilson E.M., Diwan A., Spinale F.G., and Mann D.L. Duality of innate stress responses in cardiac injury, repair, and remodeling. J Mol Cell Cardiol 37 (2004) 801-811
38. Hiasa K.I., Egashira K., Kitamoto S., Ishibashi M., Inoue S., Ni W., et al. Bone marrow mononuclear cell therapy limits myocardial infarct size through vascular endothelial growth factor. Basic Res Cardiol 99 (2004) 165-172