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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genes expressed in age-induced mitochondrial DNA deletion mutation containing / Electron Transport abnormal cells

ABSTRACT: Muscle tissue was longitudinally characterized histologically for electron transport function by staining 1mm of quadriceps muscle at 70 micron intervals for the activities of two complexes in the mitochondrial electron transport chain, Cytochrome C Oxidase and Succinate Dehydrogenase. Unstained serial cryosections were prepared for Laser Capture Microdissection. Target cells from the serial sections were isolated and pooled for RNA extraction, amplification and hybridization on Affymetrix microarrays. We selected homogeneous populations of muscle fibers for expression profiling based upon the presence/absence of electron transport dysfunction caused by the somatic accumulation of mitochondrial DNA deletion mutations. The design of this experiment is limited by the source tissue which is individually identified cells harboring intracellular clonal expansions of mitochondrial DNA deletion mutations. These unique and rare cells were identified in rat Vastus lateralis tissue in an aged 36-month old F344xBN F1 hybrid rat by exhaustive serial sectioning and subsequent histological characterization. Unstained serial sections where isolated by LCM and the purified RNA was amplified by 2 rounds of RNA based transcription prior to fragmentation and hybridization on rat genome affymetrix chips. Two populations of cells were analyzed, Electron transport deficient and normal control cells from the same animal.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Allen Herbst

PROVIDER: E-GEOD-35607 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genes expressed in age-induced mitochondrial DNA deletion mutation containing / Electron Transport abnormal cells

Project description:Muscle tissue was longitudinally characterized histologically for electron transport function by staining 1mm of quadriceps muscle at 70 micron intervals for the activities of two complexes in the mitochondrial electron transport chain, Cytochrome C Oxidase and Succinate Dehydrogenase. Unstained serial cryosections were prepared for Laser Capture Microdissection. Target cells from the serial sections were isolated and pooled for RNA extraction, amplification and hybridization on Affymetrix microarrays. We selected homogeneous populations of muscle fibers for expression profiling based upon the presence/absence of electron transport dysfunction caused by the somatic accumulation of mitochondrial DNA deletion mutations.

2013-03-01 | GSE35607 | GEO

Progressive loss of PGC-1alpha expression in aging muscle potentiates glucose intolerance and systemic inflammation

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Metabolic reprogramming during hyperammonemia targets mitochondrial function and post-mitotic senescence

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2021-11-22 | PXD027754 | Pride

Progressive loss of PGC-1alpha expression in aging muscle potentiates glucose intolerance and systemic inflammation

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Mitochondrial responses during hyperammonemia

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Transcription profiling of Arabidopis leaves from plants treated with antimycin A to trigger mitochondrial production of reactive oxygen species

Project description:mitochondrial electron transport in Arabidopsis leaves was blocked by antimycin A treatment to trigger mitochondrial production of reactive oxygen species and to study transcriptional changes in response

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Project description:Influx of Ca2+ across the inner mitochondrial membrane via the mitochondrial Ca2+ uniporter (MCU) enhances the activity of several electron transport chain dehydrogenases and the F1F0 ATP synthase. In this study, we investigated the role of MCUb, an MCU complex gene product that is a direct inhibitor of MCU mediated Ca2+ influx. We find MCUb expression to be induced by caloric restriction in heart, skeletal muscle, liver and kidney where it functions as a metabolic activator of mitochondrial fatty acid utilization. Mice selectively deficient for Mcub in skeletal muscle showed a metabolic signature of deficient fatty acid utilization in muscle, associated with progressive age-related obesity, glucose intolerance and metabolic syndrome. To define transcriptional changes underlying, and potentially contributing to this regulation of Ca2+-dependent mitochondrial fatty acid utilization, microarray analyses of tibialis anterior (TA) muscle from control and knockout mice was carried out. We used microarrays to elucidate effects of MCU and MCUb ablation on transcriptional profiles of TA muscle

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