Abstracts
Résumé
À l’inverse des cellules non musculaires (cellules vasculaires, endothéliales et musculaires lisses, présentes dans la circulation coronaire, fibroblastes en charge du réseau de collagène assurant un rôle de soutien majeur pour coordonner les éléments contractiles), les cellules musculaires cardiaques adultes sont dans un stade postmitotique. En dépit de différentes annonces, ce « dogme », ancien, ne semble pas sérieusement ébranlé. Mais on peut noter au stade terminal de l’insuffisance cardiaque l’apparition de nouvelles cellules aussi bien de type endothélial que myocytaire. Cette régénération trouve son origine soit dans des cellules souches préexistantes, soit dans des cellules progénitrices circulantes provenant de la moelle osseuse ou de l’endothélium vasculaire. Ces dernières colonisent les organes transplantés, au sein desquels on peut les voir former des chimères. Ce processus adaptatif peut être complété en injectant dans le myocarde, ou dans la circulation coronaire, divers types de cellules. Deux types sont surtout utilisés, les cellules de la moelle osseuse et les myoblastes (ou cellules satellites) du muscle squelettique. Les premières applications cliniques après infarctus du myocarde ont montré la faisabilité de la technique et les possibilités d’amélioration de la fonction contractile cardiaque.
Summary
Adult cardiac myocytes do not divide anymore. Mechanically overloaded hearts undergo hypertrophy and then fail. Cardiac hypertrophy is mainly caused by myocyte hypertrophy without myocyte proliferation, except during end-stage heart failure. By contrast, non muscular myocardial cells, such as the endothelial cells of the vessels, not only hypertrophy but are also able to proliferate. Recent works have suggested that these new cells are likely to be progenitor cells originating from bone marrow or vascular endothelium. These cells may form chimeras in the donor heart following heart transplantation. It is possible to mimic such an adaptative process by injecting progenitor cells either within the myocardium, or through the coronary circulation. Two type of cells have been utilised so far, namely bone marrow cells and myoblasts (or satellite cells) from skeletal muscles. The first clinical applications after myocardial infarction have been recently reported and showed the safety of the procedure and the possibility of improving myocardial function.
Appendices
Références
- 1. Menasché P, Hagège AA, Scorsin M, et al. First successful clinical myoblast transplantation for heart failure. Lancet 2001 ; 357 : 279-80.
- 2. Itescu S, Schuster MD, Kocher AA. New directions in strategy using cell therapy for heart disease. J Mol Med 2003 ; 81 : 288-96.
- 3. Adler CP, Sandritter W. Alterations of substances in experimentally induced cardiac hypertrophy. Basic Res Cardiol 1980 ; 75 : 126-38.
- 4. von Hardsorf R, Poole-Wilson P, Dietz R. Regenerative capacity of the myocardium : Implication for treatment of heart failure. Lancet 2004 ; 363 : 1306-13.
- 5. Grove D, Nair KG, Zak R. Biochemical correlates of cardiac hypertrophy. III. Changes in DNA content ; the relative contributions of polyploidy and mitotic activity. Circ Res 1969 ; 25 : 463-71.
- 6. Astorri E, Bolognesi R, Colla B, et al. LV hypertrophy : A cytometric study on 42 human hearts. J Mol Cell Cardiol 1977 ; 9 : 763-75.
- 7. Linzbach AJ. Heart failure from the point of view of quantitative anatomy. Am J Cardiol 1960 ; 5 : 370-81.
- 8. Swynghedauw B. Molecular mechanisms of myocardial remodeling. Physiol Rev 1999 ; 79 : 215-62.
- 9. Kajstura J, Leri A, Finato N, et al. Myocyte proliferation in end-stage cardiac failure in humans. Proc Natl Acad Sci USA 1998 ; 95 : 8801-5.
- 10. Beltrami AP, Urbanek K, Kajstura J, et al. Evidence that human cardiac myocytes divide after myocardial infarction. N Engl J Med 2001 ; 344 : 1750-7.
- 11. Limana F, Urbanek K, Chimenti S, et al. Bcl-2 overexpression promotes myocyte proliferation. Proc Natl Acad Sci USA 2002 ; 99 : 6257-62.
- 12. Weber KT. Wound healing in cardiovascular disease. Armonk, NY : Futura Publishing Cy, 1995.
- 13. Swynghedauw B. Developmental and functional adaptation of contractile proteins in cardiac and skeletal muscles. Physiol Rev 1986 ; 710 : 710-71.
- 14. Anderson DJ, Gage FH, Weissman Il. Can stem cells cross lineage boundaries ? Nat Med 2001 ; 7 : 393-5.
- 15. Oh H, Bradfute SB, Gallardo TD, et al. Cardiac progenitor cells from adult myocardium : homing, differentiation, and fusion after infarction. Proc Natl Acad SciUSA 2003 ; 100 : 12313-8.
- 16. Olson EN, Schneider MD. Sizing up the heart : Development redux in disease. Genes Dev 2003 ; 17 : 1-20.
- 17. Beltrami AP, Barlucchi L, Torella D, et al. Adult cardiac stem cells are multipotent and support myocardial regeneration. Cell 2003 ; 114 : 763-76.
- 18. Urbanek K, Quaini F, Tasca G, et al. Intense myocyte formation from cardiac stem cells in human cardiac hypertrophy. Proc Natl Acad Sci USA 2003 ; 100 : 10440-5.
- 19. Asahara T, Murohara T, Sullivan A, et al. Isolation of putative progenitor endothelial cells for angiogenesis. Science 1997 ; 275 : 964-7.
- 20. Hill JM, Zalos G, Halcox JPJ, et al. Circulating endothelial progenitors cells, vascular function, and cardiovascular risk. N Engl J Med 2003 ; 348 : 593-600.
- 21. Glaser R, Lu MM, Narula N, Epstein JA. Smooth muscle cells, but not myocytes, of host origin in transplanted human hearts. Circulation 2002 ; 106 : 17-9.
- 22. Taylor DA, Hruban R, Rodriguez ER, et al. Cardiac chimerism as a mechanism for self-repair. Does-it happen and if so to what degree ? Circulation 2002 ; 106 : 2-4.
- 23. Laflamme MA, Myerson D, Saffitz JE, et al. Evidence for cardiomyocyte repopulation by extracardiac progenitors in transplanted human hearts. Circ Res 2002 ; 90 : 634-40.
- 24. Quaini F, Urbanek K, Beltrami AP, et al. Chimerism of the transplanted heart. N Engl J Med 2002 ; 346 : 5-15.
- 25. Orlic D, Kajstura J, Chimenti S, et al. Bone marrow cells regenerate infarcted myocardium. Nature 2001 ; 410 : 701-5.
- 26. Orlic D, Kajstura J, Chimenti, et al. Mobilised bone marrow cells repairs the infarcted heart, improving function and survival. Proc Natl Acad Sci USA 2001 ; 98 : 10344-9.
- 27. Kamihata H, Matsubara H, Nishiue T, et al. Implantation of bone marrow mononuclear cells into ischemic myocardium enhances collateral perfusion and regional function via side supply of angioblasts, angiogenic ligands, and cytokines. Circulation 2001 ; 104 : 1046-52.
- 28. Kocher AA, Schuster MD, Szabolcs MJ, et al. Neovascularization of ischemic myocardium by human bone-marrow-derived angioblasts prevents cardiomyocyte apoptosis reduces remodeling and improves cardiac function. Nat Med 2001 ; 7 : 430-6.
- 29. Assmus B, Schächinger V, Teupe C, et al. Transplantation of progenitors cells and regeneration enhancement in acute myocardial infarction (TOPCARE-AMI). Circulation 2002 ; 106 : 3009-15.