Participation of the mitochondrial genome in the differentiation of neuroblastoma cells

Vayssière, Jean-Luc; Cordeau-Lossouarn, Laurence; Larcher, Jean Christophe; Basseville, Monique; Gros, François; Croizat, Bernard

doi:10.1007/bf02631065

Cited by 94 publications

(62 citation statements)

References 44 publications

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“…Indeed, inhibition of mitochondrial gene expression induces a potent decrease in cell proliferation (1,2). In addition, studies done in erythroleukemia, neurons, or myoblasts established that impairment of organelle activity also inhibits cell differentiation (3)(4)(5). Our own studies provided evidence that the latter influence resulted from actual regulation of differentiation by mitochondrial activity through the control of myogenin expression (5).…”

Section: Introductionmentioning

confidence: 93%

Stimulation of Mitochondrial Activity by p43 Overexpression Induces Human Dermal Fibroblast Transformation

et al. 2005

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Mitochondrial dysfunctions are frequently reported in cancer cells, but their direct involvement in tumorigenesis remains unclear. To understand this relation, we stimulated mitochondrial activity by overexpression of the mitochondrial triiodothyronine receptor (p43) in human dermal fibroblasts. In all clones, this stimulation induced morphologic changes and cell fusion in myotube-like structures associated with the expression of several muscle-specific genes (Myf 5, desmin, connectin, myosin, AchRa). In addition, these clones displayed all the in vivo and in vitro features of cell transformation. This phenotype was related to an increase in c-Jun and c-Fos expression and extinction of tumor suppressor gene expression (p53, p21 WAF1 , Rb 3 ). Lastly, reactive oxygen species (ROS) production was increased in positive correlation to the stimulation of mitochondrial activity. The direct involvement of mitochondrial activity in this cell behavior was studied by adding chloramphenicol, an inhibitor of mitochondrial protein synthesis, to the culture medium. This inhibition resulted in partial restoration of the normal phenotype, with the loss of the ability to fuse, a strong decrease in musclespecific gene expression, and potent inhibition of the transformed phenotype. However, expression of tumor suppressor genes was not restored. Similar results were obtained by using N-acetylcysteine, an inhibitor of ROS production. These data indicate that stimulation of mitochondrial activity in human dermal fibroblasts induces cell transformation through events involving ROS production. (Cancer Res 2005; 65(10): 4282-91)

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Section: Introductionmentioning

confidence: 93%

Stimulation of Mitochondrial Activity by p43 Overexpression Induces Human Dermal Fibroblast Transformation

et al. 2005

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“…As just discussed, mitochondria play pivotal roles in eukaryotic cells in producing cellular energy and essential metabolites as well as in controlling apoptosis by integrating various death signals (294). Mitochondrial protein synthesis inhibition, either by deleting mtDNA or by blocking translation in the organelle, is associated with the impairment of differentiation in different cell types, including neurons (390). Loss of neuronal differentiation can lead to an incomplete development of the neuron, which would result in reduced neurotransmission.…”

Section: Ead Carbonylated Proteinsmentioning

confidence: 99%

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Butterfield

Perluigi

Reed

et al. 2012

Antioxidants & Redox Signaling

156

142

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Several studies demonstrated that oxidative damage is a characteristic feature of many neurodegenerative diseases. The accumulation of oxidatively modified proteins may disrupt cellular functions by affecting protein expression, protein turnover, cell signaling, and induction of apoptosis and necrosis, suggesting that protein oxidation could have both physiological and pathological significance. For nearly two decades, our laboratory focused particular attention on studying oxidative damage of proteins and how their chemical modifications induced by reactive oxygen species/reactive nitrogen species correlate with pathology, biochemical alterations, and clinical presentations of Alzheimer's disease. This comprehensive article outlines basic knowledge of oxidative modification of proteins and lipids, followed by the principles of redox proteomics analysis, which also involve recent advances of mass spectrometry technology, and its application to selected age-related neurodegenerative diseases. Redox proteomics results obtained in different diseases and animal models thereof may provide new insights into the main mechanisms involved in the pathogenesis and progression of oxidativestress-related neurodegenerative disorders. Redox proteomics can be considered a multifaceted approach that has the potential to provide insights into the molecular mechanisms of a disease, to find disease markers, as well as to identify potential targets for drug therapy. Considering the importance of a better understanding of the cause/effect of protein dysfunction in the pathogenesis and progression of neurodegenerative disorders, this article provides an overview of the intrinsic power of the redox proteomics approach together with the most significant results obtained by our laboratory and others during almost 10 years of research on neurodegenerative disorders since we initiated the field of redox proteomics. Antioxid. Redox Signal. 17, 1610-1655.

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“…Furthermore, the general activity of the organelle, not restricted to energy production, is implicated in such regulation (Grégoire et al 1984, Buchet & Godinot 1998. Lastly, mitochondrial protein synthesis inhibition is associated with the impairment of differentiation in different cell types, such as mouse erythroleukaemia (Kaneko et al 1988) and mastocytoma cells (Laeng et al 1988), neurons (Vayssière et al 1992), and human (Herzberg et al 1993), avian (Korohoda et al 1993) or murine myoblasts (Hamai et al 1997). In agreement with this set of data, mt-TFA gene knock-out in mice is associated with embryonic lethality (Larsson et al 1998).…”

Section: Physiological Importance Of the Direct Mitochondrial T3 Pathwaymentioning

confidence: 99%

Thyroid hormone action in mitochondria

Wrutniak‐Cabello¹,

Casas²,

Cabello³

2001

Journal of Molecular Endocrinology

275

175

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Triiodothyronine (T3) is considered a major regulator of mitochondrial activity. In this review, we show evidence of the existence of a direct T3 mitochondrial pathway, and try to clarify the respective importance of the nuclear and mitochondrial pathways for organelle activity. Numerous studies have reported short-term and delayed T3 stimulation of mitochondrial oxygen consumption. Convincing data indicate that an early influence occurs through an extra-nuclear mechanism insensitive to inhibitors of protein synthesis. Although it has been shown that diiodothyronines could actually be T3 mediators of this short-term influence, the detection of specific T3-binding sites, probably corresponding to a 28 kDa c-Erb A 1 protein of the inner membrane, also supports a direct T3 influence. The more delayed influence of thyroid hormone upon mitochondrial respiration probably results from mechanisms elicited at the nuclear level, including changes in phospholipid turnover and stimulation of uncoupling protein expression, leading to an increased inner membrane proton leak. However, the involvement of a direct mitochondrial T3 pathway leading to a rapid stimulation of mitochondrial protein synthesis has to be considered.Both pathways are obviously involved in the T3 stimulation of mitochondrial genome transcription. First, a 43 kDa c-Erb A 1 protein located in the mitochondrial matrix (p43), acting as a potent T3-dependent transcription factor of the mitochondrial genome, induces early stimulation of organelle transcription. In addition, T3 increases mitochondrial TFA expression, a mitochondrial transcription factor encoded by a nuclear gene. Similarly, the stimulation of mitochondriogenesis by thyroid hormone probably involves both pathways. In particular, the c-erb A gene simultaneously encodes a nuclear and a mitochondrial T3 receptor (p43), thus ensuring coordination of the expression of the mitochondrial genome and of nuclear genes encoding mitochondrial proteins.Recent studies concerning the physiological importance of the direct mitochondrial T3 pathway involving p43 led to the conclusion that it is not only involved in the regulation of fuel metabolism, but also in the regulation of cell differentiation. As the processes leading to or resulting from differentiation are energy-consuming, p43 coordination of metabolism and differentiation could be of significant importance in the regulation of development.

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Participation of the mitochondrial genome in the differentiation of neuroblastoma cells

Cited by 94 publications

References 44 publications

Stimulation of Mitochondrial Activity by p43 Overexpression Induces Human Dermal Fibroblast Transformation

Stimulation of Mitochondrial Activity by p43 Overexpression Induces Human Dermal Fibroblast Transformation

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Thyroid hormone action in mitochondria

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