Aude Lafoux's research while affiliated with University of Nantes and other places

Publications (36)

Article
Pannexins are plasma membrane heptameric channels mediating ATP release from the cytosol to the extracellular space. Skeletal muscle activity is associated with Pannexin 1 (Panx1) channels activation, ATP release out to the extracellular space and subsequent activation of purinergic signaling pathways. In agreement, recent evidence has shown molecu...
Article
Full-text available
Duchenne muscular dystrophy (DMD) is a muscle wasting disorder caused by mutations in the gene encoding dystrophin. Gene therapy using micro-dystrophin (MD) transgenes and recombinant adeno-associated virus (rAAV) vectors hold great promise. To overcome the limited packaging capacity of rAAV vectors, most MD do not include dystrophin carboxy-termin...
Article
Full-text available
Photoactivatable drugs targeting ligand-gated ion channels open up new opportunities for light-guided therapeutic interventions. Photoactivable toxins targeting ion channels have the potential to control excitable cell activities with low invasiveness and high spatiotemporal precision. As proof-of-concept, we develop HwTxIV-Nvoc, a UV light-cleavab...
Article
Full-text available
Background Duchenne muscular dystrophy (DMD) is an X-linked inherited disease caused by mutations in the gene encoding dystrophin that leads to a severe and ultimately life limiting muscle-wasting condition. Recombinant adeno-associated vector (rAAV)-based gene therapy is promising, but the size of the full-length dystrophin cDNA exceeds the packag...
Article
Full-text available
The transient receptor potential vanilloid 1 (TRPV1) belongs to the transient receptor potential superfamily of sensory receptors. TRPV1 is a non-selective cation channel permeable to Ca2+ that is capable of detecting noxious heat temperature and acidosis. In skeletal muscles, TRPV1 operates as a reticular Ca2+-leak channel and several TRPV1 mutati...
Article
Full-text available
Duchenne Muscular Dystrophy (DMD) is a severe muscle-wasting disease caused by mutations in the DMD gene encoding dystrophin, expressed mainly in muscles but also in other tissues like retina and brain. Non-progressing cognitive dysfunction occurs in 20 to 50% of DMD patients. Furthermore, loss of expression of the Dp427 dystrophin isoform in the b...
Article
Full-text available
Corticosteroids (CS) are standard therapy for the treatment of Duchenne's muscular dystrophy (DMD). Even though they decrease inflammation, they have limited efficacy and are associated with significant side effects. There is therefore the need for new protolerogenic treatments to replace CS. Dystrophin-deficient rats (Dmd mdx ) closely resemble th...
Article
Immunological characterization of a rat model of Duchenne’s disease and demonstration of improved muscle strength after anti-CD45RC antibody treatment
Preprint
Duchenne muscular dystrophy (DMD) has as standard pharmacological therapy with corticoisteroids (CS) that decrease inflammation and immune responses present in patients and animal models. CS have however limited efficacy and important and numerous side effects. Therefore, there is a need for new anti-inflammatory and pro-tolerogenic treatments that...
Article
Full-text available
Valeriana officinalis L. root extracts are traditionally taken for their sedative and anxiolytic properties and are also used for muscle relaxation. Relaxant effects were clearly observed on smooth muscle whereas data on effects on skeletal muscle are scarce and inconsistent. The aim of this study was to assess whether a standardized extract (SE) o...
Article
Full-text available
Aging is associated with a loss of muscle mass and functional capacity. Present study was designed to compare the impact of specific dairy proteins on muscular function with or without a low-intensity physical activity program on a treadmill in an aged rat model. We investigated the effects of nutritional supplementation, five days a week over a 2-...
Article
Introduction et but de l’étude La sarcopénie est à l’origine d’une détérioration générale de l’état physique se traduisant par une perte de masse et de force musculaire conduisant à des conséquences fonctionnelles importantes telles que les troubles de la marche. L’objectif de cette étude est de comparer la force, les activités de déplacement, les...
Article
Introduction et but de l’étude L’objectif de cette étude est d’évaluer les effets de la qualité des protéines laitières administrées sous forme de bolus suite à un exercice modéré, sur la fonction locomotrice et musculaire chez le rat âgé sarcopénique. Matériel et méthodes Pendant 8 semaines, trois groupes de rats Wistar RjHan (17 mois) ont été pl...
Article
Full-text available
Sepsis, or systemic inflammatory response syndrome, is the major cause of critical illness resulting in admission to intensive care units. Sepsis is caused by severe infection and is associated with mortality in 60% of cases. Morbidity due to sepsis is complicated by neuromyopathy, and patients face long-term disability due to muscle weakness, ener...
Article
Full-text available
A few animal models of Duchenne muscular dystrophy (DMD) are available, large ones such as pigs or dogs being expensive and difficult to handle. Mdx (X-linked muscular dystrophy) mice only partially mimic the human disease, with limited chronic muscular lesions and muscle weakness. Their small size also imposes limitations on analyses. A rat model...
Article
Full-text available
Background The systemic rotenone model of Parkinson’s disease (PD) accurately replicates many aspects of the pathology of human PD, especially neurodegeneration of the substantia nigra and lesions in the enteric nervous system (ENS). Nevertheless, the precise effects of oral rotenone on the ENS have not been addressed yet. This study was therefore...
Article
Duchenne muscular dystrophy, a genetic disease caused by the absence of functional dystrophin, remains without adequate treatment. Although great hopes are attached to gene and cell therapies, identification of active small molecules remains a valid option for new treatments. We have studied the effect of 20 approved pharmaceutical compounds on the...
Article
In dystrophin-deficient skeletal muscle cells, in which Ca2+ homeostasis is disrupted and reactive oxygen species production is increased, we hypothesized that hypochlorous acid (HOCl), a strong H2O2-related free radical, damages contractile proteins and the sarcoplasmic reticulum. The aim of the present study was to investigate the effects of expo...
Article
Full-text available
The aim of this study was to investigate the effects of adenosine on reverse mode Na+/Ca(2+) exchange. In intact ferret cardiac trabeculae, Na+-free contractures were investigated after treating preparations with ryanodine, a sarcoplasmic reticulum Ca(2+) -channel inhibitor, and thapsigargin, a sarcoplasmic reticulum Ca(2+) -pump inhibitor added to...
Article
We have previously reported that CD34(+) cells purified from mouse fetal muscles can differentiate into skeletal muscle in vitro and in vivo when injected into muscle tissue of dystrophic mdx mice. In this study, we investigate the ability of such donor cells to restore dystrophin expression, and to improve the functional muscle capacity of the ext...
Article
Full-text available
The aim of the present study was to investigate the direct effects of a reactive oxygen species, H(2)O(2), on the contractile function and sarcoplasmic reticulum properties of dystrophin-deficient diaphragm using chemically skinned fibers and sarcoplasmic reticulum vesicle preparations. The results obtained using Triton X-100-skinned fibers demonst...
Article
In this study, it was shown that adenosine potentiates caffeine-induced Ca2+ release. It was then proposed that the enhancement of the caffeine-induced Ca2+ release might occur by a direct effect on the ryanodine Ca2+ release channel or on other Ca2+ regulation mechanisms. Furthermore, A2A receptors may be functional on the ferret cardiac sarcoplas...

Citations

... A recent study in this issue of Gene Therapy by Bourdon et al. [9] showed for the first time the therapeutical impact of the inclusion of the CT domain in MD construct for gene therapy. As a small animal model, the authors used the recently established DMD mdx rat model [10], which was further proven to be a suitable model to study both cardiac and vascular dysfunction in DMD [11]. ...
... Interestingly, for the force transducer platform, we found that the tetanic-to-twitch ratio was significantly higher in human muscle compared to C2C12 muscle constructs (unpaired t-test, p < 0.05). We are uncertain about the relevance of this finding, but it is likely an intrinsic feature related to the species since gender-specific differences have been found for this parameter in native mouse muscles (Lafoux et al., 2020). Of note, this parameter is independent of CSA and provides a functional measurement that could be used to compare different studies regardless of the construct size or platform used. ...
... Intending to identify the possible insults in the motor and executive networks, we observe that Dp140 + shows higher network integrity than Dp140-as the intra-network connections in the motor and executive areas are significantly higher (supplementary Fig. 1). Our results support the earlier work using fMRI analysis on sensory and motor regions in DMD [36], as well as animal models focusing on sensorimotor cortical abnormalities [37,38]. ...
... In CXMD J dogs, dystrophic changes of myocardium were not evident up to an age of 13 months [27], but vacuolar degeneration of cardiac Purkinje fibers was observed already at age 4 months [21,28]. In addition, DMD models have been created in several other species, including rabbit [29], rat [30,31], and rhesus monkey [32]. ...
... Sedatives, muscle relaxants, and poisonous chemicals can all affect muscular strength or neuromuscular function in experimental animals [35]. Grip strength changes are suggestive of weakened muscular strength and are taken as indications of motor neurotoxicity. ...
... Rat is also the animal model of choice to mimic the conditions like breast cancer and human reproduction. Different varieties of rats are available which are used for laboratory research and provide different qualities (Huchet et al., 2017). These varieties are discussed in the following subsections. ...
... The rationale for the use of MDs to treat DMD patients is that Becker Muscular Dystrophy (BMD) patients who carry in-frame deletions that naturally produce MDs, exhibit a milder dystrophinopathy [11]. Several studies have shown bodywide expression and therapeutic efficacy of MDs in DMD animal models (mdx mice, DMD mdx rats and DMD dogs) following a single systemic administration of rAAV-MD vectors [12][13][14][15][16][17][18][19][20][21][22][23][24]. Based on these data, three clinical trials of systemic rAAV-MD gene therapy were initiated in DMD patients in the USA in 2017/2018. ...
... Mice were randomly allotted to four groups according to sex and genotype. As previously described [52], half of each group was allotted to some concurrent action program on a treadmill. In the beginning, 12-week-old male and female mice were introduced to the treadmill, which had a Plexiglas ® cover to stop their escape and offered a running surface that was 100 cm in length and 7.5 cm in width. ...
... To amplify the complete mitochondrial genome, two sets of primers (Set1 and Set2) were used to perform a special long-range PCR [42]. Set1 (forward primer, 5 -GCAACCTTCTAGGTAACGACC-3 ; reverse primer, 5 -GAGTCAATACTTGGGTGGTAC-3 ) and Set2 (forward primer, 5 -CATTGGACAAGTAGCATCCGT-3 ; reverse primer, 5 -GCCTCCGATTATGATGGGTAT-3 ) regions were amplified from 20 ng of total DNA for initial denaturation at 94 • C for 1 min followed by 23-28 cycles of 94 • C 30 s, 56 • C 45 s, 68 • C 11 min and for final elongation 72 • C for 10 min with LA Taq ® DNA Polymerase (TaKaRa Bio Inc, Kusatsu, Japan). ...