Time-based gene expression programme following diaphragm injury in a rat model

Mehiri, SN; Barreiro, Esther; Hayot, Maurice; Voyer, M; Comtois, Alain Steve; Grassino, A.; Czaika, G.

doi:10.1183/09031936.05.00047704

Cited by 8 publications

(3 citation statements)

References 59 publications

(66 reference statements)

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“…Similarly to MyoD, diaphragm myogenin protein levels in the present study were also maintained after corticosteroid treatment, and relationships between diaphragm force and fiber dimensions were also found. The implication of preserved myogenin protein levels in maintaining diaphragm force is not known because the role of myogenin in mature muscles has been principally investigated during denervation and regeneration or after muscle injury (35). However, in another rat model of mechanical ventilation during which rats were allowed to breathe spontaneously for intermittent periods, the same observation between diaphragm myogenin protein levels and diaphragm force was observed (33).…”

Section: Discussionmentioning

confidence: 99%

Effects of Acute Administration of Corticosteroids during Mechanical Ventilation on Rat Diaphragm

Maes¹,

Testelmans²,

Cadot³

et al. 2008

Am J Respir Crit Care Med

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Rationale: Mechanical ventilation is known to induce ventilatorinduced diaphragm dysfunction. Patients submitted to mechanical ventilation often receive massive doses of corticosteroids that may cause further deterioration of diaphragm function. Objectives: To examine whether the combination of 24 hours of controlled mechanical ventilation with corticosteroid administration would exacerbate ventilator-induced diaphragm dysfunction. Methods: Rats were randomly assigned to a group submitted to 24 hours of controlled mechanical ventilation receiving an intramuscular injection of saline or 80 mg/kg methylprednisolone, a group submitted to 24 hours of spontaneous breathing receiving saline, or methylprednisolone and a control group. Measurements and Main Results: The diaphragm force-frequency curve was shifted downward in the mechanical ventilation group, but this deleterious effect was prevented when corticosteroids were administered. Diaphragm cross-sectional area of type I fibers was similarly decreased in both mechanical ventilation groups while atrophy of type IIx/b fibers was attenuated after corticosteroid administration. The mechanical ventilation-induced reduction in diaphragm MyoD and myogenin protein expression was attenuated after corticosteroids. Plasma cytokine levels were unchanged while diaphragm lipid hydroperoxides were similarly increased in both mechanical ventilation groups. Diaphragmatic calpain activity was significantly increased in the mechanical ventilation group, but calpain activation was abated with corticosteroid administration. Inverse correlations were found between calpain activity and diaphragm force. Conclusions: A single high dose of methylprednisolone combined with controlled mechanical ventilation protected diaphragm function from the deleterious effects of controlled mechanical ventilation. Inhibition of the calpain system is most likely the mechanism by which corticosteroids induce this protective effect.

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Section: Discussionmentioning

confidence: 99%

Effects of Acute Administration of Corticosteroids during Mechanical Ventilation on Rat Diaphragm

Maes¹,

Testelmans²,

Cadot³

et al. 2008

Am J Respir Crit Care Med

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“…Though this is unexpected, previous work has shown CJUN to act in a similar way. Mehiri et al looked at the expression of several genes following diaphragmatic injury in a rat model including CJUN [30]. In this study, CJUN mRNA expression decreased initially post-injury, returned to baseline after 12 hours and peaked at 96 hours post-injury.…”

Section: Discussionmentioning

confidence: 74%

Molecular Mechanism of Ischaemic Preconditioning of Skeletal Muscle In Vitro

Fox

Walsh

Mulhall

2018

Cureus

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Introduction Ischaemic preconditioning (IPC) is a phenomenon whereby tissues develop an increased tolerance to ischaemia and subsequent reperfusion if first subjected to sublethal periods of ischaemia. Despite extensive investigation of IPC, the molecular mechanism remains largely unknown. Our aim was to show genetic changes that occur in skeletal muscle cells in response to IPC. Methods We established an in vitro model of IPC using a human skeletal muscle cell line. Gene expression of both control and preconditioned cells at various time points was determined. The genes examined were hypoxia-inducible factor-1 alpha (HIF-1 alpha), early growth response 1 (EGR1), JUN, and FOS. HIF-1 alpha is a marker of hypoxia. EGR1, JUN, and FOS are early response genes and may play a role in the protective responses induced by IPC. Results HIF-1 alpha was upregulated following one and two hours of simulated ischaemia (p = 0.076 and 0.841, respectively) verifying that hypoxic conditions were met using our model. Expression of EGR1 and FOS was upregulated and peaked after one hour of hypoxia (p = 0.001 and <0.00, respectively). cFOS was upregulated at two and three hours of hypoxia. IPC prior to simulated hypoxia resulted in a greater level of upregulation of EGR1, JUN and FOS genes (p = <0.00, 0.047, and <0.00 respectively). Conclusion This study has supported the use of our hypoxic model for studying IPC in vitro. IPC results in a greater upregulation of protective genes in skeletal muscle cells exposed to hypoxia than in control cells. We have demonstrated hitherto unknown molecular mechanisms of IPC in cell culture.

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“…Muscle regeneration is a highly dynamic process that involves the organized orchestration of growth factor elaboration. Among the growth factors involved in muscle regeneration, basic fibroblast growth factor (bFGF) is elaborated upon injury to stimulate the activation and proliferation of muscle satellite cells to orchestrate muscle regeneration [ 7 , 8 ]. Given the importance of bFGF to muscle regeneration, the provision of bFGF may be an important component of the treatment strategy for VML.…”

Section: Introductionmentioning

confidence: 99%

Comparative Effects of Basic Fibroblast Growth Factor Delivery or Voluntary Exercise on Muscle Regeneration after Volumetric Muscle Loss

Ayan

Chiang

et al. 2022

Bioengineering

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Volumetric muscle loss (VML) is associated with irreversibly impaired muscle function due to traumatic injury. Experimental approaches to treat VML include the delivery of basic fibroblast growth factor (bFGF) or rehabilitative exercise. The objective of this study was to compare the effects of spatially nanopatterned collagen scaffold implants with either bFGF delivery or in conjunction with voluntary exercise. Aligned nanofibrillar collagen scaffold bundles were adsorbed with bFGF, and the bioactivity of bFGF-laden scaffolds was examined by skeletal myoblast or endothelial cell proliferation. The therapeutic efficacy of scaffold implants with either bFGF release or exercise was examined in a murine VML model. Our results show an initial burst release of bFGF from the scaffolds, followed by a slower release over 21 days. The released bFGF induced myoblast and endothelial cell proliferation in vitro. After 3 weeks of implantation in a mouse VML model, twitch force generation was significantly higher in mice treated with bFGF-laden scaffolds compared to bFGF-laden scaffolds with exercise. However, myofiber density was not significantly improved with bFGF scaffolds or voluntary exercise. In contrast, the scaffold implant with exercise induced more re-innervation than all other groups. These results highlight the differential effects of bFGF and exercise on muscle regeneration.

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Time-based gene expression programme following diaphragm injury in a rat model

Cited by 8 publications

References 59 publications

Effects of Acute Administration of Corticosteroids during Mechanical Ventilation on Rat Diaphragm

Effects of Acute Administration of Corticosteroids during Mechanical Ventilation on Rat Diaphragm

Molecular Mechanism of Ischaemic Preconditioning of Skeletal Muscle In Vitro

Comparative Effects of Basic Fibroblast Growth Factor Delivery or Voluntary Exercise on Muscle Regeneration after Volumetric Muscle Loss

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