Slow‐ and fast‐twitch rat hind limb skeletal muscle phenotypes 8 months after spinal cord transection and olfactory ensheathing glia transplantation

Negredo, Pilar; Rivero, José‐Luis L.; González, Blanca; Ramón‐Cueto, Almudena; Manso, Rafael

doi:10.1113/jphysiol.2007.149120

Cited by 16 publications

(11 citation statements)

References 60 publications

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“…The extensor digitorum longus (EDL) and soleus (SOL) muscles have been widely used as representative fast and slow muscles, respectively [27,28,29,30,31]. They both are hind limb muscles and very small in size (each contains about 1000 myofibers) in mouse, thus allowing for unbiased analysis of myofiber composition and gene expression at the whole muscle level [23].…”

Section: Resultsmentioning

confidence: 99%

Myostatin facilitates slow and inhibits fast myosin heavy chain expression during myogenic differentiation

Wang

Kim

et al. 2012

Biochemical and Biophysical Research Communications

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Skeletal muscles in the limb and body trunk are composed of heterogeneous myofibers expressing different isoforms of myosin heavy chain (Myh), including type I (slow, Myh7), IIA (intermediate, Myh2), IIX (fast, Myh1) and IIB (very fast, Myh4). While the contraction force and speed of a muscle are known to be determined by the relative abundance of myofibers expressing each Myh isoform, it is unclear how specific combinations of myofiber types are formed and regulated at the cellular and molecular level. We report here that myostatin (Mstn) positively regulates slow but negatively regulates fast Myh isoforms. Mstn was expressed at higher levels in the fast muscle myoblasts and myofibers than in the slow muscle counterparts. Interestingly, Mstn knockout led to a shift of Myh towards faster isoforms, suggesting an inhibitory role of Mstn in fast Myh expression. Consistently, when induced to differentiate, Mstn null myoblasts formed myotubes preferentially expressing fast Myh. Conversely, treatment of myoblasts with a recombinant Mstn protein upregulated Myh7 but downregulated Myh4 gene expression in newly formed myotubes. Importantly, both Mstn antibody and soluble activin type 2B receptor inhibited slow Myh7 and promoted fast Myh4 expression, indicating that myostatin acts through canonical activin receptor to regulate the expression of Myh genes. These results demonstrate a role of myostatin in the specification of myofiber types during myogenic differentiation.

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Section: Resultsmentioning

confidence: 99%

Myostatin facilitates slow and inhibits fast myosin heavy chain expression during myogenic differentiation

Wang

Kim

et al. 2012

Biochemical and Biophysical Research Communications

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“…23 It was found that prolonged IGF-I treatment in mdx mice can induce muscle fibers from a fast-twitch phenotype toward the slow-twitch phenotype without a change in fiber cross areas. 22 Compared with fasttwitch muscle, slow-twitch muscle fibers are rich in mitochondria, 24 have higher oxidative capacities, 25 and therefore use ATP in a more efficient way and produce less ROS, which would cause less or no damage to muscle cells. Our finding that IGF-I is able to prevent muscle cell from H 2 O 2 -induced cell death and recover cell viability may offer a rational explanation for IGF-I conferring protection on dystrophic muscle from contraction-induced damage.…”

Section: Discussionmentioning

confidence: 99%

Pretreatment with insulin-like growth factor I protects skeletal muscle cells against oxidative damage via PI3K/Akt and ERK1/2 MAPK pathways

Yang

Hoy

Fuller

et al. 2010

Laboratory Investigation

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Oxidative stress has an important role in the pathogenesis of many muscle diseases. The major contributors to oxidative stress in muscle tissue are reactive oxygen species such as oxygen ions, free radicals, and peroxides. Insulin-like growth factor I (IGF-I) has been shown to increase muscle mass and promote muscle cell proliferation, differentiation, and survival. We, therefore, hypothesized that IGF-I might also be cytoprotective for muscle cells during oxidative stress. Exogenous hydrogen peroxide (H 2 O 2 ) was used to induce oxidative stress/damage in two types of skeletal muscle cells. Apoptotic pathways were assessed after the oxidative damage and the effects of IGF-I on oxidative stress in muscle cells were examined. Different IGF-I sub-pathways were analyzed with measurement of the expression of pro-and antiapoptotic proteins. It was found that H 2 O 2 diminishes muscle cell viability and induces a caspase-independent apoptotic cell death. Pretreatment with IGF-I protects muscle cells from H 2 O 2 -induced cell death and enhances muscle cells survival. This effect appears to result from the promotion of the anti-apoptotic protein, Bcl2. Further investigation shows that protection is via an IGF-I sub-pathway: PI3K/Akt and ERK1/2 MAPK pathways. Protecting muscle cells from oxidative damage presents a potential application in the treatment of the muscle wasting, which appears in many muscle pathologies including Duchenne muscle dystrophy and sarcopenia. Many pathological muscle conditions, such as Duchenne muscle dystrophy (DMD) and sarcopenia, have been found to be associated with an increase in oxidative stress. 1 DMD is a severe progressive X-linked muscle disease with the absence of dystrophin, a protein providing structural integrity on the muscle cell membrane. Owing to the fragility of the DMD muscle membrane, normal muscular contraction in DMD destabilizes the myocyte membrane, causing intracellular accumulation of calcium. This stimulates oxidative metabolism, which generates free radicals and triggers the key pathological processes. 2 Sarcopenia is a condition with degenerative loss of skeletal muscle mass and strength associated with ageing. Mitochondrial (Mt) production of reactive oxygen species (ROS) has been shown to increase in skeletal muscle over the course of ageing, 3 which in turn reduces bioenergetic efficiency and leads to muscle fiber atrophy/loss. 4 Although DMD and sarcopenia have different pathological properties, they share a common syndrome, that is, muscle wasting. Abundant evidence implicates oxidative stress as a potential regulator of proteolytic pathways leading to muscle wasting. 5 Oxidative stress results from the activities of the reactive compounds called ROS. ROS are natural by-products in the normal metabolism of oxygen and have important roles in cell signalling. ROS including oxygen ions, free radicals, and peroxides usually have highly reactive properties because of the presence of unpaired valence shell electrons. During physiological homeostasis overall oxidati...

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“…The paralyzed skeletal muscle of rats with spinal cord injury (SCI) undergoes atrophy that was accompanied by spontaneous locomotor function recovery [21]. However, the underlying mechanism for this phenomenon after SCI is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, EGF-induced upregulation of eIF-5A stimulated corneal epithelial cell proliferation via the PI3K/Akt signaling pathway [21]. According to KEGG database, the PI3K/ Akt signaling pathway regulates fundamental cellular functions such as transcription, translation, proliferation, growth, survival, and cell cycle.…”

mentioning

confidence: 99%

Upregulation of eIF-5A1 in the paralyzed muscle after spinal cord transection associates with spontaneous hindlimb locomotor recovery in rats by upregulation of the ErbB, MAPK and neurotrophin signal pathways

Shang

Zhao

et al. 2013

Journal of Proteomics

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Slow‐ and fast‐twitch rat hind limb skeletal muscle phenotypes 8 months after spinal cord transection and olfactory ensheathing glia transplantation

Cited by 16 publications

References 60 publications

Myostatin facilitates slow and inhibits fast myosin heavy chain expression during myogenic differentiation

Myostatin facilitates slow and inhibits fast myosin heavy chain expression during myogenic differentiation

Pretreatment with insulin-like growth factor I protects skeletal muscle cells against oxidative damage via PI3K/Akt and ERK1/2 MAPK pathways

Upregulation of eIF-5A1 in the paralyzed muscle after spinal cord transection associates with spontaneous hindlimb locomotor recovery in rats by upregulation of the ErbB, MAPK and neurotrophin signal pathways

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