High-efficiency gene electrotransfer into skeletal muscle: description and physiological applicability of a new pulse generator

Durieux, Anne-Cécile; Bonnefoy, Régis; Manissolle, Chloé; Freyssenet, Damien

doi:10.1016/s0006-291x(02)00901-4

Cited by 34 publications

(43 citation statements)

References 36 publications

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“…ACTB, ␤-actin; ARBP, acidic ribosomal phosphoprotein P0; CycA, cyclophilin A; HPRT, hypoxanthine guanine phosphoribosyl transferase; MuRF1, muscle-specific RING finger protein 1; REDD1, regulated in development and DNA damage response 1. previously described (12). The fascia and skin were then closed with sutures.…”

Section: Animals and Tissue Collectionmentioning

confidence: 99%

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Downregulation of Akt/mammalian target of rapamycin pathway in skeletal muscle is associated with increased REDD1 expression in response to chronic hypoxia

Favier

Costes

Defour

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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104

114

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Although it is well established that chronic hypoxia leads to an inexorable loss of skeletal muscle mass in healthy subjects, the underlying molecular mechanisms involved in this process are currently unknown. Skeletal muscle atrophy is also an important systemic consequence of chronic obstructive pulmonary disease (COPD), but the role of hypoxemia in this regulation is still debated. Our general aim was to determine the molecular mechanisms involved in the regulation of skeletal muscle mass after exposure to chronic hypoxia and to test the biological relevance of our findings into the clinical context of COPD. Expression of positive and negative regulators of skeletal muscle mass were explored 1) in the soleus muscle of rats exposed to severe hypoxia (6,300 m) for 3 wk and 2) in vastus lateralis muscle of nonhypoxemic and hypoxemic COPD patients. In rodents, we observed a marked inhibition of the mammalian target of rapamycin (mTOR) pathway together with a strong increase in regulated in development and DNA damage response 1 (REDD1) expression and in its association with 14-3-3, a mechanism known to downregulate the mTOR pathway. Importantly, REDD1 overexpression in vivo was sufficient to cause skeletal muscle fiber atrophy in normoxia. Finally, the comparative analysis of skeletal muscle in hypoxemic vs. nonhypoxemic COPD patients confirms that hypoxia causes an inhibition of the mTOR signaling pathway. We thus identify REDD1 as a negative regulator of skeletal muscle mass during chronic hypoxia. Translation of this fundamental knowledge into the clinical investigation of COPD shows the interest to develop therapeutic strategies aimed at inhibiting REDD1.

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Section: Animals and Tissue Collectionmentioning

confidence: 99%

“…Seven days after gene electrotransfer, SOL muscles were removed under general anesthesia. Serial transverse sections (12-m) were stained for ␤-galactosidase activity and counterstained with hematoxylin-eosin-saffron (12). FCSA was measured in transfected blue fibers and nontransfected fibers (100 fibers/condition).…”

Section: Animals and Tissue Collectionmentioning

confidence: 99%

Downregulation of Akt/mammalian target of rapamycin pathway in skeletal muscle is associated with increased REDD1 expression in response to chronic hypoxia

Favier

Costes

Defour

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

104

114

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“…Leg muscles are suitable for this approach because they are amenable to physiological modulation of their mechanical activity (18), and they are accessible to somatic transgenesis (19). The pathways of TNC action were identified by monitoring transcript expression of muscle-relevant gene ontologies (GOs) in antigravitational muscle.…”

mentioning

confidence: 99%

Mechano-regulated Tenascin-C orchestrates muscle repair

Flück

Mund²,

Schittny³

et al. 2008

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

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Tenascin-C (TNC) is a mechano-regulated, morphogenic, extracellular matrix protein that is associated with tissue remodeling. The physiological role of TNC remains unclear because transgenic mice engineered for a TNC deficiency, via a defect in TNC secretion, show no major pathologies. We hypothesized that TNC-deficient mice would demonstrate defects in the repair of damaged leg muscles, which would be of functional significance because this tissue is subjected to frequent cycles of mechanical damage and regeneration. TNC-deficient mice demonstrated a blunted expression of the large TNC isoform and a selective atrophy of fast-muscle fibers associated with a defective, fast myogenic expression response to a damaging mechanical challenge. Transcript profiling mapped a set of de-adhesion, angiogenesis, and wound healing regulators as TNC expression targets in striated muscle. Expression of these regulators correlated with the residual expression of a damagerelated 200-kDa protein, which resembled the small TNC isoform. Somatic knockin of TNC in fast-muscle fibers confirmed the activation of a complex expression program of interstitial and slow myofiber repair by myofiber-derived TNC. The results presented here show that a TNC-orchestrated molecular pathway integrates muscle repair into the load-dependent control of the striated muscle phenotype.damage ͉ expression ͉ extracellular ͉ gene therapy ͉ myogenesis

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“…The comparison with electroporation was not unexpected as several other groups, including ourselves, have shown that multiple pulses at 200 V/cm cause substantial muscle damage and that modifications to the Electroporation and other physical methods DJ Wells protocol can reduce this damage. 13,65 Secondly, the laser was focused to 2 mm under the skin whereas substantially deeper focusing would be required for percutaneous delivery to human skeletal muscle. It remains to be seen if LBGT can be significantly scaled up in studies of larger muscles or other tissues.…”

Section: Clinically Applicable Ultrasound Can Enhance Plasmid-based Gmentioning

confidence: 99%

Gene Therapy Progress and Prospects: Electroporation and other physical methods

2004

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Over the last 5 years, physical methods of plasmid delivery have revolutionized the efficiency of nonviral gene transfer, in some cases reaching the efficiencies of viral vectors. In vivo electroporation dramatically increases transfection efficiency for a variety of tissues. Other methods with clinical precedent, pressure-perfusion and ultrasound, also improve plasmid gene transfer. Alternatives such as focused laser, magnetic fields and ballistic (gene gun) approaches can also enhance delivery. As plasmid DNA appears to be a safe gene vector system, it seems likely that plasmid with physically enhanced delivery will be used increasingly in clinical trials.

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High-efficiency gene electrotransfer into skeletal muscle: description and physiological applicability of a new pulse generator

Cited by 34 publications

References 36 publications

Downregulation of Akt/mammalian target of rapamycin pathway in skeletal muscle is associated with increased REDD1 expression in response to chronic hypoxia

Downregulation of Akt/mammalian target of rapamycin pathway in skeletal muscle is associated with increased REDD1 expression in response to chronic hypoxia

Mechano-regulated Tenascin-C orchestrates muscle repair

Gene Therapy Progress and Prospects: Electroporation and other physical methods

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