Blunting effect of hypoxia on the proliferation and differentiation of human primary and rat L6 myoblasts is not counteracted by Epo

Launay, Thierry; Hagström, Luciana; Lottin-Divoux, Séverine; Marchant, Dominique; Quidu, Patricia; Favret, Fabrice; Duvallet, Alain; Darribère, Thierry; Richalet, Jean‐Paul; Beaudry, Michèle

doi:10.1111/j.1365-2184.2009.00648.x

Cited by 30 publications

(48 citation statements)

References 25 publications

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“…Intrapartum hypoxia caused structural changes in the neonatal diaphragm, significantly decreasing CSA of all fiber types. Hypoxia has been shown to increase protein degradation and attenuate protein synthesis (12) and myogenesis by reducing both muscle cell proliferation and differentiation (32). Our observations that MuRF1 and atrogin-1 mRNA were increased, products of two genes involved in the ubiquitin proteasome pathway (UPP), supports in vitro observations made in L6 muscle cells subjected to hypoxia (12).…”

Section: Discussionsupporting

confidence: 78%

Maternal creatine supplementation from mid-pregnancy protects the newborn spiny mouse diaphragm from intrapartum hypoxia-induced damage

et al. 2010

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ABSTRACT:We hypothesized that maternal creatine supplementation from mid-pregnancy would protect the diaphragm of the newborn spiny mouse from the effects of intrapartum hypoxia. Pregnant mice were fed a control or 5% creatine-supplemented diet from mid-gestation. On the day before term, intrapartum hypoxia was induced by isolating the pregnant uterus in a saline bath for 7.5-8 min before releasing and resuscitating the fetuses. Surviving pups were placed with a cross-foster dam, and diaphragm tissue was collected at 24 h postnatal age. Hypoxia caused a significant decrease in the cross-sectional area (ϳ19%) and contractile function (26.6% decrease in maximum Ca 2ϩ -activated force) of diaphragm fibers. The mRNA levels of the muscle mass-regulating genes MuRF1 and myostatin were significantly increased (2-fold). Maternal creatine significantly attenuated hypoxia-induced fiber atrophy, contractile dysfunction, and changes in mRNA levels. This study demonstrates that creatine loading before birth significantly protects the diaphragm from hypoxiainduced damage at birth. (Pediatr Res 68: 393-398, 2010)

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Section: Discussionsupporting

confidence: 78%

Maternal creatine supplementation from mid-pregnancy protects the newborn spiny mouse diaphragm from intrapartum hypoxia-induced damage

et al. 2010

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“…While the underlying mechanism cannot be determined from our results, these indicate that EPO signaling in myotubes may provide some protection to the insulin signaling cascade. Expression of the EPOR gene has been long thought to be restricted to the erythroid lineage but has since been identified in C2C12 myoblasts (Ogilvie et al 2000, Launay et al 2010, Jia et al 2012) and myotubes (Joshi et al 2011, Jia et al 2012, as well as in rat (Rotter et al 2008) and human skeletal muscle (Lundby et al 2008, Rundqvist et al 2009). Although chronic treatment with EPO in vivo resulted in increased AKT activation (Hojman et al 2009) and enhanced mitochondrial oxidative phosphorylation (Plenge et al 2012) in mouse and human skeletal muscle respectively, it is still unclear whether EPOR is functional and leads to a direct effect of EPO in muscle cells.…”

Section: Discussionmentioning

confidence: 99%

Chronic erythropoietin treatment improves diet-induced glucose intolerance in rats

Caillaud¹,

Mechta²,

Ainge³

et al. 2015

Journal of Endocrinology

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Erythropoietin (EPO) ameliorates glucose metabolism through mechanisms not fully understood. In this study, we investigated the effect of EPO on glucose metabolism and insulin signaling in skeletal muscle. A 2-week EPO treatment of rats fed with a high-fat diet (HFD) improved fasting glucose levels and glucose tolerance, without altering total body weight or retroperitoneal fat mass. Concomitantly, EPO partially rescued insulin-stimulated AKT activation, reduced markers of oxidative stress, and restored heat-shock protein 72 expression in soleus muscles from HFD-fed rats. Incubation of skeletal muscle cell cultures with EPO failed to induce AKT phosphorylation and had no effect on glucose uptake or glycogen synthesis. We found that the EPO receptor gene was expressed in myotubes, but was undetectable in soleus. Together, our results indicate that EPO treatment improves glucose tolerance but does not directly activate the phosphorylation of AKT in muscle cells. We propose that the reduced systemic inflammation or oxidative stress that we observed after treatment with EPO could contribute to the improvement of whole-body glucose metabolism.

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“…The differential effects of hypoxia by species can be observed; in a previous work we showed that in rat myoblast from the L6 line, the proliferation and differentiation slow down at 1% O 2 exposure [13]. Below 1% O 2 , the mouse myoblast differentiation is blocked in a Notch-dependent manner by activating Notch-responsive promoters and increasing the expression of direct downstream genes [4].…”

Section: Introductionmentioning

confidence: 99%

Oxygen Modulates the Glutathione Peroxidase Activity during the L6 Myoblast Early Differentiation Process

Hidalgo

Marchant

Quidu

et al. 2014

Cell Physiol Biochem

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Aim: This work aims to study the regulation of the glutathione peroxidase and catalase activities in myoblasts from the L6 line exposed to 21%, 5% and 1% O₂ during the cell differentiation. Material and Methods: Rat L6 myoblasts were grown in 1%, 5% or 21% O₂ in the presence or absence of N-acetyl cysteine. The cell proliferation was evaluated by determining the doubling time and kinetics of cultures by counting cells. The cell differentiation was analyzed by determining the myogenic fusion index using antibodies against the myosin heavy chain. The glutathione peroxidase and catalase activities were assayed. The p110-PI3K/Thr308-Akt pathway was studied using western blotting. The oxidative status of the cells was carried out by determining TBARS. Results: 5% O₂ improves the glutathione peroxidase activity, p110-PI3K/Thr308-Akt pathway and differentiation while 1% O₂ alters all these parameters compared to 21% O₂. NAC (0.5 mM) can prevent the deleterious effects of hypoxia (1% O₂) on the L6 myoblast proliferation and enhances the myoblast differentiation when exposed to 21% O₂. TBARS are reduced in 5% O₂ compared to both 21% and 1% O₂. Conclusion: The glutathione peroxidase activity and p110-PI3K/Thr308-Akt are both modulated in the same way by oxygen.

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Blunting effect of hypoxia on the proliferation and differentiation of human primary and rat L6 myoblasts is not counteracted by Epo

Abstract: The data show that exposure to hypoxic conditions (1% O(2)) of rat and human myoblasts altered their proliferation and differentiation processes. They also show that Epo is not an efficient growth factor to counteract this deleterious effect.

Cited by 30 publications

References 25 publications

Maternal creatine supplementation from mid-pregnancy protects the newborn spiny mouse diaphragm from intrapartum hypoxia-induced damage

Maternal creatine supplementation from mid-pregnancy protects the newborn spiny mouse diaphragm from intrapartum hypoxia-induced damage

Chronic erythropoietin treatment improves diet-induced glucose intolerance in rats

Oxygen Modulates the Glutathione Peroxidase Activity during the L6 Myoblast Early Differentiation Process

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