Myoblast transplantation for heart failure

Menasché, Philippe; Hagège, Albert; Scorsin, Márcio; Pouzet, Bruno; Desnos, Michel; Duboc, Denis; Schwartz, Ketty; Vilquin, Jean‐Thomas; Marolleau, Jean‐Pierre

doi:10.1016/s0140-6736(00)03617-5

Cited by 1,004 publications

(547 citation statements)

References 5 publications

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“…The feasibility of meeting this challenge was demonstrated from the report of a recent Phase I clinical study of 10 patients (Menasche et al, 2001). …”

Section: Discussionmentioning

confidence: 99%

“…196: 70-78, 2003. Several pre-clinical (Atkins et al, 1999;Hutcheson et al, 2000;Pouzet et al, 2000;Scorsin et al, 2000;Jain et al, 2001) and clinical (Menasche et al, 2001) studies have shown promise for the therapeutic application of autologous human skeletal muscle cells (HuSkMC) to mitigate the deterioration of cardiac function resulting from myocardial infarction. Cells released from skeletal muscle biopsies were propagated in vitro in these studies and injected into damaged heart tissue.…”

mentioning

confidence: 99%

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Characterization of proliferating human skeletal muscle‐derived cells in vitro: Differential modulation of myoblast markers by TGF‐β2

Stewart¹,

Masi²,

Cumming³

et al. 2003

Journal Cellular Physiology

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Adult human skeletal muscle-derived cells (HuSkMC) propagated in vitro are under investigation as a cell-based therapy for the treatment of myocardial infarction. We have characterized HuSkMC with respect to cell identity and state of differentiation as a prerequisite to their clinical use. Flow cytometric analysis of propagated HuSkMC revealed a population of cells that expressed the myoblast markers CD56 and desmin. The presence of myoblasts in these cultures was further confirmed by their capacity to form myotubes and increase creatine kinase activity when cultured in low serum conditions. The non-myoblast fraction of these propagated cells expressed TE7, a marker associated with the fibroblast phenotype. Spontaneous differentiation of myoblasts occurred during serial propagation of HuSkMC, as judged by myotube formation, thereby reducing the myoblast representative fraction with continued cell expansion. We examined transforming growth factor b2 (TGF-b2) for its utility in controlling this spontaneous differentiation of adult human myoblasts in vitro. Propagation of HuSkMC in the presence of 1 ng/ml TGFb2 for 5 days decreased desmin expression within the myoblast population and caused a parallel reduction of creatine kinase activity. CD56 expression was unaffected, indicating a differential regulation of these myoblast markers. The reduction in desmin expression and creatine kinase activity was, however, reversible upon the removal of TGF-b. These data collectively indicate that TGF-b2 restrained differentiation of adult human skeletal myoblasts during propagation without causing irreversible loss of the myoblast phenotype, demonstrating the potential utility of using TGF-b2 during cultivation and expansion of HuSkMC intended for therapeutic implantation.

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“…The feasibility of meeting this challenge was demonstrated from the report of a recent Phase I clinical study of 10 patients (Menasche et al, 2001). …”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Characterization of proliferating human skeletal muscle‐derived cells in vitro: Differential modulation of myoblast markers by TGF‐β2

Stewart¹,

Masi²,

Cumming³

et al. 2003

Journal Cellular Physiology

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“…Novel surgical therapies include left ventricular remodelling, mechanical circulatory assistance and, more recently, isolated cell transplantation or gene therapy (111)(112)(113)(114)(115)(116). The advent of cell transplantation provides great promise for the future because it may be a useful adjunct to several of the previously mentioned therapies.…”

Section: Arnold Et Almentioning

confidence: 99%

Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006: Diagnosis and management

Arnold¹,

Liu²,

Demers³

et al. 2006

Canadian Journal of Cardiology

363

256

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“…22,29 This issue is completely avoided in the context of autologous MT, which has been successfully developed as an experimental treatment for postischemic heart failure or dilated cardiomyopathy, showing its feasibility, safety and its great clinical interest. [32][33][34][35][36] In some myopathic condition such as FSHD, characterized by a relatively localized muscle involvement, and the absence of therapeutic options, autologous MT could be considered as an alternative strategy. In this case, unaffected muscles could be the source of myoblasts to be transferred into affected muscles in order to improve their regeneration ability.…”

Section: Introductionmentioning

confidence: 99%

Normal growth and regenerating ability of myoblasts from unaffected muscles of facioscapulohumeral muscular dystrophy patients

Vilquin

Sacconi

et al. 2005

Gene Ther

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Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant disease characterized by a typical regional distribution, featuring composed patterns of clinically affected and unaffected muscles. No treatment is available for this condition, in which the pathophysiological mechanism is still unknown. Autologous transfer of myoblasts from unaffected to affected territories could be considered as a potential strategy to delay or stop muscle degeneration. To evaluate the feasibility of this concept, we explored and compared the growth and differentiation characteristics of myoblasts prepared from phenotypically unaffected muscles of five FSHD patients and 10 control donors. According to a clinically approved procedure, 10 9 cells of a high degree of purity were obtained within 16-23 days. More than 80% of these cells were myoblasts, as demonstrated by labeling of the muscle markers CD56 and desmin. FSHD myoblasts presented a doubling time equivalent to that of control cells; they kept high proliferation ability and did not show early telomere shortening. In vitro, these cells were able to differentiate and to express muscle-specific antigens. In vivo, they participated to muscle structures when injected into immunodeficient mice. These data suggest that myoblasts expanded from unaffected FSHD muscles may be suitable tools in view of autologous cell transplantation clinical trials.

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Myoblast transplantation for heart failure

Cited by 1,004 publications

References 5 publications

Characterization of proliferating human skeletal muscle‐derived cells in vitro: Differential modulation of myoblast markers by TGF‐β2

Characterization of proliferating human skeletal muscle‐derived cells in vitro: Differential modulation of myoblast markers by TGF‐β2

Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006: Diagnosis and management

Normal growth and regenerating ability of myoblasts from unaffected muscles of facioscapulohumeral muscular dystrophy patients

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