Cardiac Chimerism as a Mechanism for Self-Repair

Taylor, Doris A.; Hruban, Ralph H.; Rodriguez, Erica; Goldschmidt‐Clermont, Pascal J.

doi:10.1161/01.cir.0000024386.99599.4a

Cited by 73 publications

(16 citation statements)

References 14 publications

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“…The dose of G-CSF used was a tenth lower than that in previously described studies using a murine MI model to mobilize bone marrow stem cells into the peripheral circulation. Moreover, accumulating evidence has questioned whether G-CSF induces transdifferentiation from bone marrow progenitor cells to cardiomyocytes (62)(63)(64)(65). Second, we could not exclude direct effects of CSFs on cardiomyocytes.…”

Section: Discussionmentioning

confidence: 92%

Differential Effects of GM-CSF and G-CSF on Infiltration of Dendritic Cells during Early Left Ventricular Remodeling after Myocardial Infarction

Naito

Anzai

Sugano

et al. 2008

The Journal of Immunology

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Several lines of evidence suggest that the immune activation after myocardial infarction (MI) induces secondary myocardial injury. Although dendritic cells (DC) are potent regulators of immunity, their role in MI is still undetermined. We investigated the effect of DC modulation by CSF on left ventricular (LV) remodeling after MI. MI was induced by ligation of the left coronary artery in male Wistar rats. G-CSF (20 μg/kg/day, MI-G, n = 33), a GM-CSF inducer (romurtide, 200 μg/kg/day, MI-GM, n = 28), or saline (MI-C, n = 55) was administered for 7 days. On day 14, MI-G animals had higher LV max dP/dt and smaller LV dimensions, whereas MI-GM animals had lower LV max dP/dt and larger LV dimensions than did MI-C animals, despite similar infarct size. In MI-C, OX62+ DC infiltrated the infarcted and border areas, peaking on day 7. Bromodeoxyuridine-positive DC were observed in the border area during convalescence. Infiltration by DC was decreased in MI-G animals and increased in MI-GM animals compared with MI-C (p < 0.05). In the infarcted area, the heat shock protein 70, TLR2 and TLR4, and IFN-γ expression were reduced in MI-G, but increased in MI-GM in comparison with those in MI-C animals. IL-10 expression was higher in MI-G and lower in MI-GM than in MI-C animals. In conclusion, G-CSF improves and GM-CSF exacerbates early postinfarction LV remodeling in association with modulation of DC infiltration. Suppression of DC-mediated immunity could be a new strategy for the treatment of LV remodeling after MI.

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Section: Discussionmentioning

confidence: 92%

Differential Effects of GM-CSF and G-CSF on Infiltration of Dendritic Cells during Early Left Ventricular Remodeling after Myocardial Infarction

Naito

Anzai

Sugano

et al. 2008

The Journal of Immunology

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“…131 However, it is proven that cardiomyocytes are predifferentiated cells without the proliferative capacity to regenerate, though a couple of studies in patients who suffered an acute MI suggest that there is a small number of cardiomyocytes capable of entering the cell cycle actively. 132,133 Although in vivo transplanted cardiomyocytes were found to integrate into the damaged myocardium, 127,128 the results in a porcine animal model showed that the majority of the transplanted cells were separated from host cardiomyocytes by scar tissue. 134 This is a severe drawback, as incomplete electrical conduct would lead to fatal arrhythmias.…”

Section: Cardiomyocytesmentioning

confidence: 99%

Minimally invasive cell-seeded biomaterial systems for injectable/epicardial implantation in ischemic heart disease

Ravichandran¹,

Venugopal²,

Sundarrajan³

et al. 2012

IJN

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Myocardial infarction (MI) is characterized by heart-wall thinning, myocyte slippage, and ventricular dilation. The injury to the heart-wall muscle after MI is permanent, as after an abundant cell loss the myocardial tissue lacks the intrinsic capability to regenerate. New therapeutics are required for functional improvement and regeneration of the infarcted myocardium, to overcome harmful diagnosis of patients with heart failure, and to overcome the shortage of heart donors. In the past few years, myocardial tissue engineering has emerged as a new and ambitious approach for treating MI. Several left ventricular assist devices and epicardial patches have been developed for MI. These devices and acellular/cellular cardiac patches are employed surgically and sutured to the epicardial surface of the heart, limiting the region of therapeutic benefit. An injectable system offers the potential benefit of minimally invasive release into the myocardium either to restore the injured extracellular matrix or to act as a scaffold for cell delivery. Furthermore, intramyocardial injection of biomaterials and cells has opened new opportunities to explore and also to augment the potentials of this technique to ease morbidity and mortality rates owing to heart failure. This review summarizes the growing body of literature in the field of myocardial tissue engineering, where biomaterial injection, with or without simultaneous cellular delivery, has been pursued to enhance functional and structural outcomes following MI. Additionally, this review also provides a complete outlook on the tissue-engineering therapies presently being used for myocardial regeneration, as well as some perceptivity into the possible issues that may hinder its progress in the future.

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“…La réponse vient des chimères réalisées au cours de transplantations d'organes lorsque le receveur est de sexe masculin et le donneur féminin (Figure 2). Le chromosome Y est identifiable par fluorescence au moyen de sondes ADN spécifiques comme le satellite CEP Y III, bien que cette identification ne soit pas très sensible (on ne trouve guère plus de 35% de cellules positives chez des témoins masculins [21]) et demande l'identification simultanée de la membrane basale [22]. Des cellules endothéliales chimériques sont en effet retrouvées dans le myocarde 1 à 2 semaines après transplantation [19,22].…”

Section: De La Circulation ?unclassified

“…Le chromosome Y est identifiable par fluorescence au moyen de sondes ADN spécifiques comme le satellite CEP Y III, bien que cette identification ne soit pas très sensible (on ne trouve guère plus de 35% de cellules positives chez des témoins masculins [21]) et demande l'identification simultanée de la membrane basale [22]. Des cellules endothéliales chimériques sont en effet retrouvées dans le myocarde 1 à 2 semaines après transplantation [19,22]. En revanche, pour la plupart des auteurs [19][20][21][22][23], à une exception près [24], des myocytes chimériques n'ont jamais été retrouvés en quantité notable, même plusieurs années après la transplantation.…”

Section: De La Circulation ?unclassified

“…En revanche, pour la plupart des auteurs [19][20][21][22][23], à une exception près [24], des myocytes chimériques n'ont jamais été retrouvés en quantité notable, même plusieurs années après la transplantation. L'identification de myocytes chimériques pose par ailleurs des problèmes techniques importants qui expliquent ces différences (discuté dans [22]). …”

Section: De La Circulation ?unclassified

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Le myocyte cardiaque adulte peut-il encore proliférer ?

Swynghedauw

2004

Med Sci (Paris)

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La croissance et la prolifération postnatale sont des caractéristiques essentielles des myocytes cardiaques qui permettent au coeur d'adapter progressivement sa masse à la demande hémodynamique. Mais, une fois l'âge adulte atteint, l'arrêt des divisions semble être un mal nécessaire au maintien de la stabilité des fonctions électriques et mécaniques du myocarde. Les myocytes cardiaques ont-ils toutefois gardé la capacité de proliférer ? La question est, pour plusieurs raisons, loin d'être académique. Ainsi, en cas d'infarctus du myocarde, c'est-à-dire de mort par ischémie d'un certain nombre de cellules myocardiques, la capacité conservée des myocytes à proliférer permettrait d'envisager la régénération spontanée ou provoquée de la zone infarcie, en totalité ou en partie. En revanche, en cas d'incapacité des myocytes à proliférer, la fibrose réparatrice serait la seule possibilité de limiter les dégâts, et la transplantation d'un nouveau coeur, ou l'injection de cellules progénitrices, le seul moyen de rétablir la situation [1] (‹). La capacité des myocytes cardiaques à proliférer est limitéeEn milieu de gestation, la prolifération des cardiomyocytes est de 33%, contre 2% seulement à la naissance. Karyocinèse et cytocinèse sont dissociées après la naissance et, selon les espèces, il apparaît des cellules polynucléées, binucléées le plus souvent [2], ou polyploïdes [3]. L'arrêt du cycle cellulaire est sous le contrôle de deux familles fonctionnelles distinctes de protéines kinases inhibitrices dépendant des cyclines, Ink4 et Cip/Kip, lesquelles bloquent l'activation de l'ADN polymérase [2]; peu d'informations sont disponibles sur le fonctionnement de ces deux familles d'inhibiteurs au sein du myocarde jeune ou adulte [4]. L'hypothèse d'un arrêt du cycle cellulaire a également été renforcée par le fait que la survenue d'un cancer du myocarde est exceptionnelle et, en tous les cas, jamais MEDECINE/SCIENCES 2004 ; 20 : 710-4

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Cardiac Chimerism as a Mechanism for Self-Repair

Cited by 73 publications

References 14 publications

Differential Effects of GM-CSF and G-CSF on Infiltration of Dendritic Cells during Early Left Ventricular Remodeling after Myocardial Infarction

Differential Effects of GM-CSF and G-CSF on Infiltration of Dendritic Cells during Early Left Ventricular Remodeling after Myocardial Infarction

Minimally invasive cell-seeded biomaterial systems for injectable/epicardial implantation in ischemic heart disease

Le myocyte cardiaque adulte peut-il encore proliférer ?

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