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MRNA Expression Changes Induced by Myocardial MCU Inhibition

ABSTRACT: Mitochondrial calcium is an important second-messenger controlling fight-or-flight responses in the heart. The molecular identity of MCU (Mitochondrial Calcium Uniporter) was recently discovered allowing us to test this hypothesis in vivo by expressiing a myocardial delimited dominant negative form of MCU. We queried mRNA expression changes induced by dominant negative MCU expression in the heart.

ORGANISM(S): Mus musculus

PROVIDER: GSE62049 | GEO | 2015/06/07

SECONDARY ACCESSION(S): PRJNA263029

REPOSITORIES: GEO

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mRNA Expression Changes Induced by Myocardial MCU Inhibition

Project description:Mitochondrial calcium is an important second-messenger controlling fight-or-flight responses in the heart. The molecular identity of MCU (Mitochondrial Calcium Uniporter) was recently discovered allowing us to test this hypothesis in vivo by expressing a myocardial delimited dominant negative form of MCU. We queried mRNA expression changes induced by dominant negative MCU expression in the heart. Neonatal (< 24 h) and 6 week old hearts were harvested from mice expressing the dominant negative MCU construct or wild-type littermates.

2015-06-07 | E-GEOD-62049 | biostudies-arrayexpress

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Project description:Muscle atrophy contributes to the poor prognosis of many physiopathological conditions, but pharmacological therapies are still limited. Muscle activity leads to major swings in mitochondrial [Ca2+] which control aerobic metabolism, cell death and survival pathways. We have investigated in vivo the effects of mitochondrial Ca2+ homeostasis in skeletal muscle function and trophism, by overexpressing or silencing the Mitochondrial Calcium Uniporter (MCU). The results coherently demonstrate that both in developing and in adult muscles MCU-dependent mitochondrial Ca2+ uptake has a marked trophic effect that does not depend on autophagy or aerobic control, but impinges on two major hypertrophic pathways of skeletal muscle, PGC-1M-NM-14 and Igf1-Akt/PKB. In adult mice, MCU overexpression protects from denervation-induced atrophy. These data reveal a novel Ca2+-dependent organelle-to-nucleus signaling route, which links mitochondrial function to the control of muscle mass and may represent a possible pharmacological target in sarcopenia. Experiments were performed on biological replicates of single skeletal muscle fibres. Seven fibres were chosen for their Mutochondrial Calcium Uniporter (MCU) overexpression and other seven fibres because MCU was silenced. Overexpression and silencing were performed injecting skeletal muscle with AAV containing MCU gene or short interfering oligos specific for MCU. As control was profiled eigth fibres transfected with AAV and eigth wild type fibres. Analyses were performed 7 days and 14 days after the AAV injection (3 fibers after 7 days and 4 fibers after 14 days for MCU overexpression and silencing, four fibres after 7 days and four after 14 days for control).

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The role of mitochondrial calcium in embryonal rhabdomyosarcoma

Project description:Rhabdomyosarcoma (RMS), the most common paediatric soft-tissue sarcoma, is characterized by cells of skeletal muscle origin that fail to both irreversibly exit the cell cycle and complete skeletal muscle differentiation. Embryonal rhabdomyosarcoma (ERMS) is the most prevalent subtype of RMS and its molecular signatures has been associated with metabolism defects and increased oxidative stress. However, the details of the contributing factors or molecules have not been studied. Both metabolism and oxidative stress are associated with mitochondrial functions and an important molecule that regulates mitochondrial functions is calcium. Till date, there has been no studies that examine the role of mitochondrial calcium in ERMS. In addition, the molecular component of mitochondrial calcium uniporter complex, which is responsible for the uptake of mitochondrial calcium was only discovered in 2012. Since then, there has been an increasing interest in investigating the role of mitochondrial calcium and mitochondrial calcium uniporter complex in various cancers. Mitochondrial calcium uniporter (MCU), the main channel forming protein is often found to be dysregulated in various cancers. Our preliminary data has shown that mitochondrial calcium is dysregulated in ERMS due to overexpression of MCU. This dysregulation of mitochondrial calcium has led to multiple mitochondrial dysfunctions and oncogenic phenotypes. Hence, we would like to investigate the downstream targets of MCU in order to identify the mechanism through which MCU regulates oncogenic phenotypes in ERMS.

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