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The transcriptional cascade associated with creatine kinase down-regulation and mitochondrial biogenesis in mice sarcoma

100%

Bera S., Ray M.

Cellular and Molecular Biology Letters

2009

tom 14

nr 3

481-496

The tissue-specific expressions of creatine kinase (CK) isoforms are regulated by the coordinated action of various transcription factors. The myogenic differentiation factor D (MyoD) family of proteins and the myocyte-specific enhancer binding factor 2 family of transcription factors are important in regulating the muscle-specific expression of cytosolic muscle-type CK (MCK) and mitochondrial CKs. As reported in some related studies, TNF-α mediated degradation of MyoD and myogenin mRNA may lead to severe muscle wasting and cachexia, which is characterized by a low transcript level of MCK and myosin heavy chain proteins. In our previous study, we reported on a complete loss of total CK activity and expression when sarcoma was induced in mouse skeletal muscle (Patra et al. FEBS J. 275 (2008) 3236–3247). This study aimed at investigating the transcriptional cascade of CK down-regulation in carcinogen-induced sarcoma in mouse muscle. Both CK deficiency and enhanced nitric oxide synthase (NOS) were known to augment mitochondrial biogenesis, so we also explored the activation of the transcriptional cascade of mitochondrial biogenesis in this cancer. We observed the activation of the TNF-α-mediated nitric oxide production pathway with NFκB activation and concomitant degradation of MyoD and myogenin mRNA. Exploration of mitochondrial biogenesis revealed high cytochrome c oxidase activity and mitochondrial DNA content in sarcoma. The PGC-related co-activator seems to have a major role in regulating mitochondrial biogenesis by upregulating nuclear respiratory factors and mitochondrial transcription factor A. From the above findings, it can be concluded that severe muscle degeneration leads to CK down-regulation in sarcoma, and that the stimulation of mitochondrial biogenesis indicated a scenario representing both CK deficiency and NOS overexpression on the one hand, and altered bioenergetic profiling on the other.

Prohibitins and Ras2 protein cooperate in the maintenance of mitochondrial function during yeast aging

84%

Kirchman P. A., Miceli M. V., West R. L., Jiang J. C., Kim S., Jazwinski S. M.

Acta Biochimica Polonica

2003

tom 50

nr 4

The yeast Saccharomyces cerevisiae has a finite replicative life span. Yeasts possess two prohibitins, Phb1p and Phb2p, in similarity to mammalian cells. These proteins are located in the inner mitochondrial membrane, where they are involved in the processing of newly-synthesized membrane proteins. We demonstrate that the elimination of one or both of the prohibitin genes in yeast markedly diminished the replicative life span of cells that lack fully-functional mitochondria, while having no effect on cells with functioning mitochondria. This deleterious effect was suppressed by the deletion of the RAS2 gene. The expression of PHB1 and PHB2 declined gradually up to 5-fold during the life span. Cells in which PHB1 was deleted in conjunction with the absence of a mitochondrial genome displayed remarkable changes in mitochondrial morphology, distribution, and inheritance. This loss of mi- tochondrial integrity was not seen in cells devoid of PHB1 but possessing an intact mitochondrial genome. In a subset of the cells, the changes in mitochondrial integrity were associated with increased production of reactive oxygen species, which co-localized with the altered mitochondria. The mitochondrial deficits described above were all suppressed by deletion of RAS2. Our data, together with published information, are interpreted to provide a unified view of the role of the prohibitins in yeast aging. This model posits that the key initiating event is a decline in mitochondrial function, which leads to progressive oxidative damage that is exacerbated in the absence of the prohibitins. This aggravation of the initial damage is ameliorated by the suppression of the production of mitochondrial proteins in the absence of Ras2p signaling of mitochondrial biogenesis.

Regulation by exercise of skeletal muscle content of mitochondria and GLUT4

67%

Holloszy J. O.

Journal of Physiology and Pharmacology. Supplement

2008

tom 59

nr 7

Ograniczanie wyników

1 Acta Biochimica Polonica

1 Cellular and Molecular Biology Letters

1 Journal of Physiology and Pharmacology. Supplement

1 Bera S.

1 Holloszy J. O.

1 Jazwinski S. M.

1 Jiang J. C.

1 Kim S.

1 Kirchman P. A.

1 Miceli M. V.

1 Ray M.

1 West R. L.

1 2009

1 2008

1 2003

Wyniki wyszukiwania

The transcriptional cascade associated with creatine kinase down-regulation and mitochondrial biogenesis in mice sarcoma

Prohibitins and Ras2 protein cooperate in the maintenance of mitochondrial function during yeast aging

Regulation by exercise of skeletal muscle content of mitochondria and GLUT4