P43-dependent mitochondrial activity regulates myoblast differentiation and slow myosin isoform expression by control of Calcineurin expression

Seyer, Pascal; Grandemange, Stéphanie; Rochard, Pierrick; Busson, Muriel; Pessemesse, Laurence; Casas, François; Cabello, Gérard; Wrutniak‐Cabello, Chantal

doi:10.1016/j.yexcr.2011.05.020

Cited by 37 publications

(50 citation statements)

References 49 publications

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“…Mitochondria have been recognized as crucial players in myogenesis, and a considerable body of evidence suggests that impairment of their subcellular organisation and activity blocks myogenic differentiation [15, 26, 30, 47, 48]. Our data further confirm this notion and also highlight the importance of preserving mitochondrial integrity in this differentiation process.…”

Section: Discussionsupporting

confidence: 84%

Creatine Prevents the Structural and Functional Damage to Mitochondria in Myogenic, Oxidatively Stressed C2C12 Cells and Restores Their Differentiation Capacity

Barbieri

Guescini

Calcabrini

et al. 2016

Oxidative Medicine and Cellular Longevity

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Creatine (Cr) is a nutritional supplement promoting a number of health benefits. Indeed Cr has been shown to be beneficial in disease-induced muscle atrophy, improve rehabilitation, and afford mild antioxidant activity. The beneficial effects are likely to derive from pleiotropic interactions. In accord with this notion, we previously demonstrated that multiple pleiotropic effects, including preservation of mitochondrial damage, account for the capacity of Cr to prevent the differentiation arrest caused by oxidative stress in C2C12 myoblasts. Given the importance of mitochondria in supporting the myogenic process, here we further explored the protective effects of Cr on the structure, function, and networking of these organelles in C2C12 cells differentiating under oxidative stressing conditions; the effects on the energy sensor AMPK, on PGC-1α, which is involved in mitochondrial biogenesis and its downstream effector Tfam were also investigated. Our results indicate that damage to mitochondria is crucial in the differentiation imbalance caused by oxidative stress and that the Cr-prevention of these injuries is invariably associated with the recovery of the normal myogenic capacity. We also found that Cr activates AMPK and induces an upregulation of PGC-1α expression, two events which are likely to contribute to the protection of mitochondrial quality and function.

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Section: Discussionsupporting

confidence: 84%

Creatine Prevents the Structural and Functional Damage to Mitochondria in Myogenic, Oxidatively Stressed C2C12 Cells and Restores Their Differentiation Capacity

Barbieri

Guescini

Calcabrini

et al. 2016

Oxidative Medicine and Cellular Longevity

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“…These data suggest that p43 through a mitochondrial-nuclear cross-talk regulates the expression of genes involved in the cell cycle in testis as previously described for others cells and tissues [14], [24]–[26].…”

Section: Discussionsupporting

confidence: 84%

“…c-myc is known to regulate Cdk4 and mitochondrial function [25]. This data suggesting that c-myc is an important target of mitochondrial activity is fully in line with the work of Seyer et al [26] showing that in myoblast C2C12, an inhibition of mitochondrial activity by chloramphenicol (which mimics a lack of p43) increased c-myc mRNA and protein levels. Conversely, stimulation of mitochondrial activity by overexpression of the T3 mitochondrial receptor (p43) down-regulates c-myc expression.…”

Section: Discussionsupporting

confidence: 84%

Depletion of the p43 Mitochondrial T3 Receptor Increases Sertoli Cell Proliferation in Mice

et al. 2013

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Among T3 receptors, TRα1 is ubiquitous and its deletion or a specific expression of a dominant-negative TRα1 isoform in Sertoli cell leads to an increase in testis weight and sperm production. The identification of a 43-kDa truncated form of the nuclear receptor TRα1 (p43) in the mitochondrial matrix led us to test the hypothesis that this mitochondrial transcription factor could regulate Sertoli cell proliferation. Here we report that p43 depletion in mice increases testis weight and sperm reserve. In addition, we found that p43 deletion increases Sertoli cell proliferation in postnatal testis at 3 days of development. Electron microscopy studies evidence an alteration of mitochondrial morphology observed specifically in Sertoli cells of p43−/− mice. Moreover, gene expression studies indicate that the lack of p43 in testis induced an alteration of the mitochondrial-nuclear cross-talk. In particular, the up-regulation of Cdk4 and c-myc pathway in p43−/− probably explain the extended proliferation recorded in Sertoli cells of these mice. Our finding suggests that T3 limits post-natal Sertoli cell proliferation mainly through its mitochondrial T3 receptor p43.

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“…P43 is a mitochondrial T3 receptor ubiquitously expressed which stimulates mitochondrial transcription and protein synthesis in the presence of T3 [5]. In avian QM7 myoblasts or murine C2C12 cells, p43 overexpression stimulates mitochondrial activity and potentiates terminal differentiation whereas direct inhibition of this pathway induces the reverse changes [6], [7], [8]. In vivo , we have shown that p43 overexpression in skeletal muscle increases mitochondrial DNA content, mitochondrial respiration, and induces a shift in metabolic and contractile features of muscle fibers towards a slower and more oxidative phenotype [9].…”

Section: Introductionmentioning

confidence: 99%

Mice Lacking the p43 Mitochondrial T3 Receptor Become Glucose Intolerant and Insulin Resistant during Aging

et al. 2013

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Thyroid hormones (TH) play an important regulatory role in energy expenditure regulation and are key regulators of mitochondrial activity. We have previously identified a mitochondrial triiodothyronine (T3) receptor (p43) which acts as a mitochondrial transcription factor of the organelle genome, which leads in vitro and in vivo, to a stimulation of mitochondrial biogenesis. Recently, we generated mice carrying a specific p43 invalidation. At 2 months of age, we reported that p43 depletion in mice induced a major defect in insulin secretion both in vivo and in isolated pancreatic islets, and a loss of glucose-stimulated insulin secretion. The present study was designed to determine whether p43 invalidation influences life expectancy and modulates blood glucose and insulin levels as well as glucose tolerance or insulin sensitivity during aging. We report that from 4 months old onwards, mice lacking p43 are leaner than wild-type mice. p43−/− mice also have a moderate reduction of life expectancy compared to wild type. We found no difference in blood glucose levels, excepted at 24 months old where p43−/− mice showed a strong hyperglycemia in fasting conditions compared to controls animals. However, the loss of glucose-stimulated insulin secretion was maintained whatever the age of mice lacking p43. If up to 12 months old, glucose tolerance remained unchanged, beyond this age p43−/− mice became increasingly glucose intolerant. In addition, if up to 12 months old p43 deficient animals were more sensitive to insulin, after this age we observed a loss of this capacity, culminating in 24 months old mice with a decreased sensitivity to the hormone. In conclusion, we demonstrated that during aging the depletion of the mitochondrial T3 receptor p43 in mice progressively induced an increased glycemia in the fasted state, glucose intolerance and an insulin-resistance several features of type-2 diabetes.

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P43-dependent mitochondrial activity regulates myoblast differentiation and slow myosin isoform expression by control of Calcineurin expression

Cited by 37 publications

References 49 publications

Creatine Prevents the Structural and Functional Damage to Mitochondria in Myogenic, Oxidatively Stressed C2C12 Cells and Restores Their Differentiation Capacity

Creatine Prevents the Structural and Functional Damage to Mitochondria in Myogenic, Oxidatively Stressed C2C12 Cells and Restores Their Differentiation Capacity

Depletion of the p43 Mitochondrial T3 Receptor Increases Sertoli Cell Proliferation in Mice

Mice Lacking the p43 Mitochondrial T3 Receptor Become Glucose Intolerant and Insulin Resistant during Aging

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