Study of postmyocardial infarction scar-formation mechanisms: Advantage of an experimental myocardial infarction model in mice;Étude des mécanismes de cicatrisation après infarctus du myocarde: Intérêt d'un modèle expérimental d'infarctus du myocarde chez la souris

Canadian Journal of Cardiology

Volumn 20, Issue 14, 2004, Pages 1467-1475

  Barandon, Laurent ^a,b,c   Couffinhal, Thierry ^a,b   Dufourcq, Pascale ^b   Daret, Danièle ^b   Allières, Cécile ^b   Alzieu, Philippe ^b   Deville, Claude ^a   Duplàa, Cécile ^b  

^a HAUT LÉVÊQUE HOSPITAL   (France)

^b INSERM   (France)

^c MONTREAL HEART INSTITUTE   (Canada)

Author keywords

[No Author keywords available]

Indexed keywords

COLLAGEN;

ANGIOGENESIS; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTERY LIGATION; ARTICLE; CELL DIFFERENTIATION; CELL PROLIFERATION; CONTROLLED STUDY; EXTRACELLULAR MATRIX; GENE TARGETING; GRANULATION TISSUE; HEART HEMODYNAMICS; HEART INFARCTION; HEART INFARCTION SIZE; HEART LEFT VENTRICLE CONTRACTILITY; HEART LEFT VENTRICLE CONTRACTION; HEART LEFT VENTRICLE FUNCTION; HEART LEFT VENTRICLE PRESSURE; HEART LEFT VENTRICLE RELAXATION; HEART RUPTURE; INFLAMMATION; LEFT ANTERIOR DESCENDING CORONARY ARTERY; MALE; MORTALITY; MOUSE; MYOFIBROBLAST; NEUTROPHIL; NONHUMAN; SCAR FORMATION; TISSUE REPAIR; TRANSGENIC MOUSE; ANIMAL; C57BL MOUSE; CORONARY BLOOD VESSEL; DISEASE MODEL; FEMALE; HEART VENTRICLE REMODELING; PATHOLOGY; PHYSIOLOGY; POSTOPERATIVE COMPLICATION; RISK FACTOR; SCAR; SENSITIVITY AND SPECIFICITY; SURVIVAL;

ANIMALS; CICATRIX; CORONARY VESSELS; DISEASE MODELS, ANIMAL; FEMALE; HEART RUPTURE, POST-INFARCTION; MALE; MICE; MICE, INBRED C57BL; MYOCARDIAL INFARCTION; POSTOPERATIVE COMPLICATIONS; RISK FACTORS; SENSITIVITY AND SPECIFICITY; SURVIVAL ANALYSIS; VENTRICULAR FUNCTION, LEFT; VENTRICULAR REMODELING;

EID: 12144270411     PISSN: 0828282X     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (32)

1. Sun Y, Weber KT. Infarct scar: A dynamic tissue. Cardiovasc Res 2000;46:250-6.
2. Cleutjens JP, Blankesteijn WM, Daemen MJ, et al. The infarcted myocardium: Simply dead tissue, or a lively target for therapeutic interventions. Cardiovasc Res 1999;44:232-41.
3. Weber KT. Infarcted hearts of mice and men. Cardiovasc Res 1999;41:506-8.
4. Yu Z, Redfern CS, Fishman GT. Conditional transgene expression in the heart. Circ Res 1996;79:691-7.
5. Barandon L, Couffinhal T, Dufourcq P, et al. Frizzled A, a novel angiogenic factor: Promises for cardiac repair. Eur J Cardiothorac Surg 2004;25:76-83.
6. Barandon L, Couffinhal T, Ezan J, et al. Reduction of infarct size and prevention of cardiac rupture in transgenic mice overexpressing FrzA. Circulation 2003;108:2282-9.
7. Couffinhal T, Silver M, Zheng LP, et al. Mouse model of angiogenesis. Am J Pathol 1998;152:1667-79.
8. Dufourcq P, Couffinhal T, Ezan J, et al. FrzA, a secreted frizzled related protein, induced angiogenic response. Circulation 2002;106:3097-103.
9. MacIntyre K, Capewell S, Stewart S, et al. Evidence of improving prognosis in heart failure: Trends in case fatality in 66 547 patients hospitalized between 1986 and 1995. Circulation 2000;102:1126-31.
10. Patten RD, Aronovitz MJ, Deras-Mejia L, et al. Ventricular remodeling in a mouse model of myocardial infarction. Am J Physiol 1998;274:H1812-20.
11. Li Q, Li B, Wang X, et al. Overexpression of insulin-like growth factor-1 in mice protects from myocyte death after infarction, attenuating ventricular dilation, wall stress, and cardiac hypertrophy. J Clin Invest 1997;100:1991-9.
12. Misra A, Haudek SB, Knuefermann P et al. Nuclear factor-kappaB protects the adult cardiac myocyte against ischemia-induced apoptosis in a murine model of acute myocardial infarction. Circulation 2003;108:3075-8.
13. Shiomi T, Tsutsui H, Matsusaka H, et al. Overexpression of glutathione peroxidase prevents left ventricular remodeling and failure after myocardial infarction in mice. Circulation 2004;109:544-9.
14. Kaiser RA, Bueno OF, Lips DJ, et al. Targeted inhibition of p38 MAPK antagonizes cardiac injury and cell death following ischemia-reperfusion in vivo. J Biol Chem 2004;279:15524-30.
15. Bao W, Hu E, Tao L, et al. Inhibition of Rho-kinase protects the heart against ischemia/reperfusion injury. Cardiovasc Res 2004;61:548-58.
16. Zou Y, Zhu W, Sakamoto M, et al. Heat shock transcription factor 1 protects cardiomyocytes from ischemia/reperfusion injury. Circulation 2003;108:3024-30.
17. Kang YJ, Li Y, Sun X. Antiapoptotic effect and inhibition of ischemia/reperfusion-induced myocardial injury in metallothionein-overexpressing transgenic mice. Am J Pathol 2003;163:1579-86.
18. Briaud SA, Ding ZM, Michael LH, et al. Leukocyte trafficking and myocardial reperfusion injury in ICAM-1/P- selectin-knockout mice. Am J Physiol Heart Circ Physiol 2001;280:H60-7.
19. Frangogiannis NG, Smith CW, Entman ML. The inflammatory response in myocardial infarction. Cardiovasc Res 2002;53:31-47.
20. Cleutjens JP. The role of matrix metalloproteinases in heart disease. Cardiovasc Res 1996;32:816-21.
21. Lindsey ML, Gannon J, Aikawa M, et al. Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction. Circulation 2002;105:753-8.
22. Ducharme A, Frantz S, Aikawa M, et al. Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction. J Clin Invest 2000;106:55-62.
23. Heymans S, Luttun A, Nuyens D, et al. Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure. Nat Med 1999;5:1135-42.
24. Nelissen-Vrancken HJ, Debets JJ, Snoeckx LH, et al. Time-related normalization of maximal coronary flow in isolated perfused hearts of rats with myocardial infarction. Circulation 1996;93:349-55.
25. MacKenna D, Summerour SR, Villarreal FJ. Role of mechanical factors in modulating cardiac fibroblast function and extracellular matrix synthesis. Cardiovasc Res 2000;46:257-63.
26. Gabbiani O. Evolution and clinical implications of the myofibroblast concept. Cardiovasc Res 1998;38:545-8.
27. Blankesteijn WM, Essers-Janssen YP, Verluyten MJ, et al. A homologue of Drosophila tissue polarity gene frizzled is expressed in migrating myofibroblasts in the infarcted rat heart. Nat Med 1997;3:541-4.
28. Blankesteijn WM, van Gijn ME, Essers-Janssen YP, et al. Beta-catenin, an inducer of uncontrolled cell proliferation and migration in malignancies, is localized in the cytoplasm of vascular endothelium during neovascularization after myocardial infarction. Am J Pathol 2000;157:877-83.
29. Hwang MW, Matsumori A, Furukawa Y, et al. Neutralization of interleukin-1beta in the acute phase of myocardial infarction promotes the progression of left ventricular remodeling. J Am Coll Cardiol 2001;38:1546-53.
30. Olivetti O, Capasso JM, Sonnenblick EH, et al. Side-to-side slippage of myocytes participates in ventricular wall remodeling acutely after myocardial infarction in rats. Circ Res 1990;67:23-34.
31. Yang Z, Bove CM, French BA, et al. Angiotensin II type 2 receptor overexpression preserves left ventricular function after myocardial infarction. Circulation 2002;106:106-11.
32. Takeshita K, Hayashi M, Iino S, et al. Increased expression of plasminogen activator inhibitor-1 in cardiomyocytes contributes to cardiac fibrosis after myocardial infarction. Am J Pathol 2004;164:449-56.