Specific features of satellite cells and myoblasts at different stages of rat postnatal development

Balan, O. V.; Vorotelyak, E. A.; Смирнова, Т. Д.; Ozernyuk, N. D.

doi:10.1134/s1062359008020052

Cited by 6 publications

(2 citation statements)

References 18 publications

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“…Satellite cells were essential for muscle regeneration, which was activated, proliferated, differentiated into myotubes, and ultimately fused with existing myofibers to participate in muscle regeneration (Tidball, 2011;Relaix and Zammit, 2012). In this study, we found that Pax7, the specific marker of satellite (Balan et al, 2008;Relaix and Zammit, 2012), did not change in the whole process of injured muscle regeneration. And it was not affected by CL-liposomes treatment.…”

Section: Discussionmentioning

confidence: 60%

Macrophage depletion impairs skeletal muscle regeneration: The roles of regulatory factors for muscle regeneration

Liu

Zhao

et al. 2017

Cell Biology International

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Though macrophages are essential for skeletal muscle regeneration, which is a complex process, the roles and mechanisms of the macrophages in the process of muscle regeneration are still not fully understood. The objective of this study is to explore the roles of macrophages and the mechanisms involved in the regeneration of injured skeletal muscle. One hundred and twelve C57BL/6 mice were randomly divided into muscle contusion and macrophages depleted groups. Their gastrocnemius muscles were harvested at the time points of 12 h, 1, 3, 5, 7, 14 d post-injury. The changes in skeletal muscle morphology were assessed by hematoxylin and eosin (HE) stain. The gene expression was analyzed by real-time polymerase chain reaction. The data showed that CL-liposomes treatment did affect the expression of myogenic regulatory factors (MyoD, myogenin) after injury. In addition, CL-liposomes treatment decreased the expression of regulatory factors of muscle regeneration (HGF, uPA, COX-2, IGF-1, MGF, FGF6) and increased the expression of inflammatory cytokines (TGF-β1, TNF-α, IL-1β, RANTES) in the late stage of regeneration. Moreover, there were significant correlations between macrophages and some regulatory factors (such as HGF, uPA) for muscle regeneration. These results suggested that macrophages depletion impairs skeletal muscle regeneration and that the regulatory factors for muscle regeneration may play important roles in this process.

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Section: Discussionmentioning

confidence: 60%

Macrophage depletion impairs skeletal muscle regeneration: The roles of regulatory factors for muscle regeneration

Liu

Zhao

et al. 2017

Cell Biology International

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“…Myoblasts are the resident stem cells of skeletal muscle and are relatively quiescent in resting conditions. Upon activation, myoblasts proliferate, differentiate, and fuse into mature myotubes, which is necessary for the development and adaptive reconstruction of skeletal muscle tissue (Balan, Voroteliak, Smirnova, & Ozerniuk, ; Burattini et al, ). Mechanical loading has been reported in promoting the skeletal muscle remodeling (Collinsworth et al, ; Goldspink et al, ; Vandenburgh, Hatfaludy, Karlisch, & Shansky, ; Vandenburgh, Swasdison, & Karlisch, ).…”

Section: Introductionmentioning

confidence: 99%

Cleavage of caspase‐12 at Asp94, mediated by endoplasmic reticulum stress (ERS), contributes to stretch‐induced apoptosis of myoblasts

Song

Zhang

Wang

et al. 2018

Journal Cellular Physiology

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Mechanical overloading can lead to skeletal muscle damage instead of remodeling. This is attributed to the excessive apoptosis of myoblasts, mechanism of which remains to be elucidated. The present study aimed to investigate the involvement of endoplasmic reticulum stress (ERS) and caspase-12 in mediating the stretch-induced apoptosis of myoblasts. Myoblast apoptosis was evaluated by Hoechst staining, DNA fragmentation assay, Annexin V binding, and propidium iodide staining, as well as caspase-3 and poly-ADP-ribose polymerase 1 cleavage. First, our results showed that apoptosis was elevated in a time-dependent manner when myoblasts were subjected to cyclic mechanical stretch (CMS) for 12, 24, and 36 hr. Concomitantly, CMS triggered the ERS and caspase-12 cleavage; ERS inhibitor GSK 2606414 suppressed the CMS-induced cleavage of caspase-12 and myoblast apoptosis. Silencing caspase-12 attenuated the apoptosis of myoblasts under CMS. Furthermore, CMS-induced myoblast apoptosis was partially recovered by overexpressing wild-type caspase-12 in caspase-12-silenced myoblasts. In contrast, overexpressing mutant caspase-12 (D94N), which cannot be cleaved into the active caspase-12 fragments, failed to accomplish the same effect. Finally, C2C12 overexpressing truncated caspase-12 segment (TC-casp12-D94), which starts from Asp94 and ends at Asn419, underwent apoptosis under both static and stretched conditions. Interestingly, C2C12 myoblasts seemed to be resistant to stretch-induced apoptosis upon low-serum-induced differentiation. In conclusion, our study provided evidence that caspase-12 cleavage at Asp94, induced by ERS under mechanical stimuli, is the key molecule in initiating the stretch-triggered apoptosis of myoblasts.

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Analysis of expression of heavy myosin chains during in vitro differentiation of satellite cells and myoblasts derived from rat skeletal muscles

Balan

Myuge

Ozernyuk

2009

Biol Bull Russ Acad Sci

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Specific features of satellite cells and myoblasts at different stages of rat postnatal development

Cited by 6 publications

References 18 publications

Macrophage depletion impairs skeletal muscle regeneration: The roles of regulatory factors for muscle regeneration

Macrophage depletion impairs skeletal muscle regeneration: The roles of regulatory factors for muscle regeneration

Cleavage of caspase‐12 at Asp94, mediated by endoplasmic reticulum stress (ERS), contributes to stretch‐induced apoptosis of myoblasts

Analysis of expression of heavy myosin chains during in vitro differentiation of satellite cells and myoblasts derived from rat skeletal muscles

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