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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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE35607 | GEO | 2013/03/01

SECONDARY ACCESSION(S): PRJNA152533

REPOSITORIES: GEO

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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. 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.

2013-03-01 | E-GEOD-35607 | biostudies-arrayexpress

Mitochondrial electron transport chain is necessary for NLRP3 inflammasome activation

Project description:Mitochondrial electron transport chain is necessary for NLRP3 inflammasome activation

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Rewiring the Mitochondrial Electron Transport Chain Enhances Tumor Immunogenicity

Project description:Although tumor growth requires the mitochondrial electron transport chain (ETC), the relative contribution of Complex I (CI) and II (CII), the gatekeepers for initiating electron flow, remains unclear. Here, we report that loss of CII, but not CI, reduces melanoma tumor growth by increasing antigen presentation and T cell-mediated killing. This is driven by succinate-mediated transcriptional and epigenetic activation of major histocompatibility complex I-antigen processing and presentation (MHC-APP) genes that is independent of interferon signaling. Furthermore, knock-out of MCJ, to promote electron entry preferentially via CI, provides proof-of-concept of ETC rewiring to achieve anti-tumor responses without side effects associated with an overall reduction in mitochondrial respiration in non-cancer cells. Our results hold therapeutic potential for tumors that have reduced MHC-APP expression, a common mechanism of cancer immunoevasion.

2024-05-01 | GSE235311 | GEO

Rewiring the Mitochondrial Electron Transport Chain Enhances Tumor Antigen Presentation and Immunogenicity [bulk RNA-seq]

Project description:Loss of antigen presentation by MHCI is a common mechanism of tumor immune evasion. Mitochondrial oxidative phosphorylation (OXPHOS) capacity influences MHCI expression, but the underlying molecular mechanisms remain unclear. Here, we demonstrate that the relative flow of electrons through complex I or II of the mitochondrial electron transport chain (ETC) regulates MHCI expression and antigen presentation in cancer cells. Specifically, reducing electron flow from complex II increases mitochondrial succinate which activates transcription of MHCI and antigen processing and presentation (APP) genes. These phenotypes are independent of the interferon (IFN) signaling pathway and driven by succinate-mediated enzymatic inhibition of lysine-specific demethylases, KDM5A/B and destabilization of polycomb repressor complex 2 (PRC2). Finally, knockout of the mitochondrial Complex I inhibitor protein, MCJ, preferentially reduces electron flow through Complex II and increases succinate which drives an enhanced antigen-dependent CD8+ T cell response to mouse melanoma tumors in vivo. These findings suggest that the mitochondrial ETC can be manipulated therapeutically to enhance antitumor immune responses independently of IFNγ.

2022-12-31 | GSE198346 | GEO

Mitochondrial electron transport chain is necessary for NLRP3 inflammasome activation

Project description:The NLRP3 inflammasome is linked to sterile and pathogen-dependent inflammation, and its dysregulation underlies many chronic diseases. Mitochondria have been implicated as regulators of NLRP3 inflammasome through multiple mechanisms including generation of mitochondrial ROS. Here we report that mitochondrial electron transport chain (ETC) complexes I, II, III and V inhibitors all prevent NLRP3 inflammasome activation. Ectopic expression of Saccharomyces cerevisiae NADH dehydrogenase (NDI1) or Ciona intestinalis alternative oxidase (AOX), which can respectively complement the functional loss of mitochondrial complex I or III, without generation of ROS, rescued NLRP3 inflammasome activation in the absence of endogenous mitochondrial complex I or complex III function. Metabolomics revealed phosphocreatine (PCr), which can sustain ATP levels, as a common metabolite that is diminished by mitochondrial ETC inhibitors. PCr depletion decreased ATP levels and NLRP3 inflammasome activation. Thus, mitochondrial ETC sustains NLRP3 inflammasome activation through PCr-dependent generation of ATP but a ROS independent mechanism.

2022-03-09 | GSE197606 | GEO

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

Project description:Decreased mitochondrial mass and function in muscle of diabetic patients is associated with low PGC-1alpha, a transcriptional coactivator of the mitochondrial gene program. To investigate whether reduced PGC-1alpha and oxidative capacity in muscle directly contributes to age-related glucose intolerance, we compared the genetic signatures and metabolic profiles of aging mice lacking muscle PGC-1alpha. Microarray analysis revealed that a significant proportion of PGC-1alpha-dependent changes in gene expression overlapped with age-associated effects, and aging muscle and muscle lacking PGC-1alpha shared gene signatures of impaired electron transport chain activity and TGFbeta signalling. Gastrocnemius muscle mRNA from young (10 week old) and old (24 month old) wild-type and knock-out (muscle-specific PGC-1alpha, myogenin-cre) C57Bl/6N/6J/129 mice

2013-12-05 | E-GEOD-52550 | biostudies-arrayexpress

Rewiring the Mitochondrial Electron Transport Chain Enhances Tumor Antigen Presentation and Immunogenicity [bulk RNA-seq]

Project description:Rewiring the Mitochondrial Electron Transport Chain Enhances Tumor Antigen Presentation and Immunogenicity [bulk RNA-seq]

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

2013-12-05 | GSE52550 | GEO

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

2010-12-31 | E-TABM-641 | biostudies-arrayexpress

Antimycin A treatment of Arabidopsis leaves in a PrxII F knockout

Project description:Mitochondrial electron transport in Arabidopsis leaves was blocked by antimycin A treatment to trigger mitochondrial production of reactive oxygen species in a knockout line for a mitochondrial peroxidase (PrxII F) and to study transcriptional changes in response

2011-11-01 | E-TABM-1196 | biostudies-arrayexpress

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