Regeneration of muscles after cardiotoxin injury I. Cytological aspects

Couteaux, R; Mira, Jean‐Claude; d’Albis, Anne

doi:10.1111/j.1768-322x.1988.tb00719.x

Cited by 114 publications

(78 citation statements)

References 25 publications

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“…To further investigate the SC function within the engineered muscle, we used a cardiotoxin (CTX) injury assay to assess whether the SCs can support muscle self-repair in vitro. Homeostatic, 2-wk-old engineered muscle was exposed to 0.2 μM CTX for 6 h and allowed to recover for 10 d. Consistent with in vivo reports (28), the CTX exposure resulted in immediate fragmentation of myofibers, cell death, and disruption of contractile elements, leading to a fourfold decrease in contractile-force generation ( Fig. 2 and SI Appendix, Fig.…”

Section: /Myodsupporting

confidence: 56%

Biomimetic engineered muscle with capacity for vascular integration and functional maturation in vivo

Juhas

Engelmayr

Fontanella

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

212

316

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Tissue-engineered skeletal muscle can serve as a physiological model of natural muscle and a potential therapeutic vehicle for rapid repair of severe muscle loss and injury. Here, we describe a platform for engineering and testing highly functional biomimetic muscle tissues with a resident satellite cell niche and capacity for robust myogenesis and self-regeneration in vitro. Using a mouse dorsal window implantation model and transduction with fluorescent intracellular calcium indicator, GCaMP3, we nondestructively monitored, in real time, vascular integration and the functional state of engineered muscle in vivo. During a 2-wk period, implanted engineered muscle exhibited a steady ingrowth of blood-perfused microvasculature along with an increase in amplitude of calcium transients and force of contraction. We also demonstrated superior structural organization, vascularization, and contractile function of fully differentiated vs. undifferentiated engineered muscle implants. The described in vitro and in vivo models of biomimetic engineered muscle represent enabling technology for novel studies of skeletal muscle function and regeneration.tissue engineering | contractile force | self-repair | angiogenesis | window chamber

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Section: /Myodsupporting

confidence: 56%

Biomimetic engineered muscle with capacity for vascular integration and functional maturation in vivo

Juhas

Engelmayr

Fontanella

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

212

316

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“…Here, we modified a previously described animal model (22,45) and showed extensive and complete regeneration in vivo as assessed by morphology, DNA replication, and mRNA expression profiles. Microarray and semiquantitative RT-PCR analyses and comparison between normal and irradiated muscles in this regeneration model define new insights into molecular events important for control of proliferation and differentiation in satellite cells in vivo.…”

Section: Discussionmentioning

confidence: 99%

Highly Coordinated Gene Regulation in Mouse Skeletal Muscle Regeneration

Yan

Choi

Liu

et al. 2003

Journal of Biological Chemistry

238

227

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Mammalian skeletal muscles are capable of regeneration after injury. Quiescent satellite cells are activated to reenter the cell cycle and to differentiate for repair, recapitulating features of myogenesis during embryonic development. To understand better the molecular mechanism involved in this process in vivo, we employed high density cDNA microarrays for gene expression profiling in mouse tibialis anterior muscles after a cardiotoxin injection. Among 16,267 gene elements surveyed, 3,532 elements showed at least a 2.5-fold change at one or more time points during a 14-day time course. Hierarchical cluster analysis and semiquantitative reverse transcription-PCR showed induction of genes important for cell cycle control and DNA replication during the early phase of muscle regeneration. Subsequently, genes for myogenic regulatory factors, a group of imprinted genes and genes with functions to inhibit cell cycle progression and promote myogenic differentiation, were induced when myogenic stem cells started to differentiate. Induction of a majority of these genes, including E2f1 and E2f2, was abolished in muscles lacking satellite cell activity after gamma radiation. Regeneration was severely compromised in E2f1 null mice but not affected in E2f2 null mice. This study identifies novel genes potentially important for muscle regeneration and reveals highly coordinated myogenic cell proliferation and differentiation programs in adult skeletal muscle regeneration in vivo.Skeletal muscles are damaged and repaired repeatedly throughout life. Muscle regeneration maintains locomotor function during aging and delays the appearance of clinical symptoms in neuromuscular diseases, such as Duchenne muscular dystrophy (1, 2). This capacity for tissue repair is conferred by satellite cells located between the basal lamina and the sarcolemma of mature myofibers (3, 4). Upon injury, satellite cells reenter the cell cycle, proliferate, and then exit the cell cycle either to renew the quiescent satellite cell pool or to differentiate into mature myofibers (5). Understanding the molecular mechanism by which satellite cell activity is regulated could promote development of novel countermeasures to enhance muscle performance that is compromised by diseases or aging.Both the cell proliferation and differentiation programs are essential for myogenesis. Mammalian cells escape from quiescence (G 0 ) and enter the cell cycle by activating the Cdk 1 /Rb/ E2f signaling pathway (6, 7). In general, mitogen stimulation induces expression and assembly of the G 1 cyclin-dependent kinases (Cdks) (8, 9). Activation of Cdks causes phosphorylation of the retinoblastoma protein (Rb) (10, 11), leading to increased activities of a subset of E2f transcription factors (E2fs) (12) and up-regulation of a variety of E2f-responsive genes encoding proteins directly involved in DNA replication and cell cycle progression (13,14). On the other hand, myogenic differentiation is controlled by interactions of a network of myogenic transcription factors (15). Studies ...

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“…Tibialis muscle was injected with 0.1 ml of 10 M cardiotoxin (Calbiochem), which was diluted in PBS (14,15). Muscle was harvested at various times after injection (1, 2, 3, 4, 7, 14, and 30 days).…”

Section: Methodsmentioning

confidence: 99%

Muscle regeneration in the prolonged absence of myostatin

Wagner

Liu

Chang

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

176

123

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Myostatin is an endogenous inhibitor of muscle conserved across diverse species. In the absence of myostatin, there is massive muscle growth in mice, cattle, and humans. Previous studies in the mdx mouse model of muscular dystrophy demonstrate that inhibiting myostatin attenuates several features of dystrophic muscle. These findings have encouraged the development of human therapies to block myostatin. However, little is known of the long-term effects on muscle of myostatin blockade. To evaluate potential sequelae from the prolonged absence of myostatin, senescent myostatin null (mstn ؊/؊ ) mice were studied. Senescent mstn ؊/؊ mice continue to have normal muscle with increased mass and strength relative to controls. Muscles of senescent mstn ؊/؊ mice regenerate robustly from both chronic and acute injury. Early markers of regeneration are enhanced in the absence of myostatin, suggesting a mechanism for the attenuation of dystrophic features found in mdx mice lacking myostatin.aging ͉ muscular dystrophy

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Regeneration of muscles after cardiotoxin injury I. Cytological aspects

Cited by 114 publications

References 25 publications

Biomimetic engineered muscle with capacity for vascular integration and functional maturation in vivo

Biomimetic engineered muscle with capacity for vascular integration and functional maturation in vivo

Highly Coordinated Gene Regulation in Mouse Skeletal Muscle Regeneration

Muscle regeneration in the prolonged absence of myostatin

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