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Expression profiles of C2C12 myotubes in response to PGC-1M-NM-1 (peroxisome proliferator-activated receptor gamma, coactivator 1 alpha) overexpression and/or iron chelation

ABSTRACT: Mitochondria are centers of metabolism and signaling whose content and function must adapt to changing cellular environments. The biological signals that initiate mitochondrial restructuring and the cellular processes that drive this adaptive response are largely obscure. To better define these systems, we performed matched quantitative genomic and proteomic analyses of mouse muscle cells as they performed mitochondrial biogenesis. We find that proteins involved in cellular iron homeostasis are highly coordinated with this process, and that depletion of cellular iron results in a rapid, dose-dependent decrease of select mitochondrial protein levels and oxidative capacity. We further show that this process is universal across a broad range of cell types and fully reversed when iron is reintroduced. Collectively, our work reveals that cellular iron is a key regulator of mitochondrial biogenesis, and provides quantitative datasets that can be leveraged to explore post-transcriptional and post-translational processes that are essential for mitochondrial adaptation. C2C12 mouse myoblasts were differentiated into myotubes for 3 days, at which point they were infected with adenovirus expressing either green fluorescent protein (GFP) or GFP-tagged PGC-1M-NM-1 (GFP-PGC-1M-NM-1) M-BM-1 treatment with the iron chelator deferoxamine (DFO) (for 4 treatments total). The cells were grown for three more days, then RNA was extracted and applied to Affymetrix Mouse 430 2.0 arrays. Gene expression was measured in biological duplicate (4 treatments M-CM-^W 2 replicates = 8 arrays).

ORGANISM(S): Mus musculus

SUBMITTER: David Pagliarini

PROVIDER: E-GEOD-42299 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression profiles of C2C12 myotubes in response to PGC-1α (peroxisome proliferator-activated receptor gamma, coactivator 1 alpha) overexpression and/or iron chelation

Project description:Mitochondria are centers of metabolism and signaling whose content and function must adapt to changing cellular environments. The biological signals that initiate mitochondrial restructuring and the cellular processes that drive this adaptive response are largely obscure. To better define these systems, we performed matched quantitative genomic and proteomic analyses of mouse muscle cells as they performed mitochondrial biogenesis. We find that proteins involved in cellular iron homeostasis are highly coordinated with this process, and that depletion of cellular iron results in a rapid, dose-dependent decrease of select mitochondrial protein levels and oxidative capacity. We further show that this process is universal across a broad range of cell types and fully reversed when iron is reintroduced. Collectively, our work reveals that cellular iron is a key regulator of mitochondrial biogenesis, and provides quantitative datasets that can be leveraged to explore post-transcriptional and post-translational processes that are essential for mitochondrial adaptation.

2012-12-10 | GSE42299 | GEO

Change expression of genes in iron chelation and deficient conditions

Project description:Firstly, cell senescence and anti-oxidant genes were down-regulated by iron deficient mice and iron-specific chelator deferoxamine (DFO) using a DNA microarray. Our data suggested that down-regulation of anti-oxidant genes and cell senescence gene induced oxidative stress in iron-deficient and -specific chelated condition.

2018-01-26 | GSE109656 | GEO

PGC-1 alpha Mediates Differentiation of Mesenchymal Stem Cells toward Brown Adipose Cells

Project description:Mesenchymal stem cells (MSCs) are a multipotent cell type that can differentiate into non-hematopoietic cells, such as adipocytes. Adipocyte tissue is central to regulate energy balance. PGC-1 alpha controls several aspects of mitochondrial biogenesis. However, roles of PGC-1 alpha in brown fat differentiation of MSCs remain uncertain. To investigate roles of PGC-1 alpha in brown fat differentiation immortalized human MSCs were used for all experiments. The changes in genetic profiling between MSCs and PGC-1 alpha-expressing MSCs were analyzed by microarray analysis. The genetic profiling of PGC-1 alpha-expressing MSCs shows the significant increase of genes related to mitochondrial functions and lipid metabolism compared to that of MSCs. When expressed in MSCs, PGC-1 alpha activates a robust mitochondrial biogenesis and respiration. The expression of thermogenic markers, such as cytochrome C and complex II, was significantly increased in MSCs with treatment of adenovirus expressing PGC-1 alpha. Our microarray results also indicate that genetic pattern of PGC-1 alpha-expressing MSCs is very closed to that of adipose tissues. Bone marrow-derived MSCs were infected with Ad-GFP, or Ad-PGC-1? at a multiplicity of infection (m.o.i.) of 500 overnight.

2010-12-01 | E-GEOD-19643 | biostudies-arrayexpress

Transcriptional network analysis in muscle reveals AP-1 as a partner of PGC-1M-NM-1 in the regulation of the hypoxic gene program [microarray: PGC1a_vs_GFP]

Project description:Skeletal muscle tissue shows an extraordinary cellular plasticity, but the underlying molecular mechanisms are still poorly understood. Here we use a combination of experimental and computational approaches to unravel the complex transcriptional network of muscle cell plasticity centered on the peroxisome proliferator-activated receptor M-NM-3 coactivator 1M-NM-1 (PGC-1M-NM-1), a regulatory nexus in endurance training adaptation. By integrating data on genome-wide binding of PGC-1M-NM-1 and gene expression upon PGC-1M-NM-1 over-expression with comprehensive computational prediction of transcription factor binding sites (TFBSs), we uncover a hitherto underestimated number of transcription factor partners involved in mediating PGC-1M-NM-1 action. In particular, principal component analysis of TFBSs at PGC-1M-NM-1 binding regions predicts that, besides the well-known role of the estrogen-related receptor M-NM-1 (ERRM-NM-1), the activator protein-1 complex (AP-1) plays a major role in regulating the PGC-1M-NM-1-controlled gene program of hypoxia response. Our findings thus reveal the complex transcriptional network of muscle cell plasticity controlled by PGC-1M-NM-1. We used microarrays to detect changes in gene expression in C2C12 cells following PGC-1alpha over-expression or GFP (control) over-expression. We used 3 biological replicates for each condition.

2014-06-16 | E-GEOD-51189 | biostudies-arrayexpress

Transcription profiling of mouse myoblasts (C2C12 cells) differentiated into myotubes infected with an adenovirus expressing either green fluorescent protein (GFP) or PGC-1alpha, known to induce mitochondrial biogenesis in muscle cells

Project description:Microarray time-course of mouse myotubes transduced with the transcriptional co-activator PGC-1alpha, which is known to induce mitochondrial biogenesis in muscle cells. Experiment Overall Design: Cultured mouse myoblasts (C2C12 cells) were differentiated into myotubes and on day 3 were infected with an adenovirus expressing either green fluorescent protein (GFP) or PGC-1alpha. Gene expression was measured at three time points (days 0, 1, 2, 3) in biological triplicate.

2007-12-11 | E-GEOD-4330 | biostudies-arrayexpress

Pyruvate induces mitochondrial biogenesis by a PGC-1alpha independent mechanism

Project description:The present study examines the impact of altering energy provision on mitochondrial biogenesis in muscle cells. C2C12 myoblasts were chronically treated with supraphysiological levels of sodium pyruvate for 72 hr. Treated cells exhibited increased mitochondrial protein expression, basal respiratory rate and maximal oxidative capacity. The increase in mitochondrial biogenesis was independent of increases in PGC-1alpha and PGC-1alpha mRNA expression. To further assess whether PGC-1alpha expression was necessary for pyruvate action, cells were infected with adenovirus containing shRNA for PGC-1alpha prior to treatment with pyruvate. Despite a 70% reduction in PGC-1alpha mRNA the effect of pyruvate was preserved. Furthermore, pyruvate induced mitochondrial biogenesis in primary myoblasts from PGC-1alpha null mice. These data suggest that regulation of mitochondrial biogenesis by pyruvate in myoblasts is independent of PGC-1alpha, suggesting the existence of a novel energy-sensing pathway regulating oxidative capacity. Keywords: basal state versus treatment at one time point

2006-08-12 | GSE5497 | GEO

Transcription profiling of differentiated brown adipocytes from wild type, PGC-1 alpha knockout, or PGC-1 alpha knockout and PGC-1 beta knockdown mice to investigate the roles of PGC-1 coactivators in brown fat differentiation.

Project description:Mitochondria play an essential role in the ability of brown fat to generate heat, and the PGC-1 coactivators control several aspects of mitochondrial biogenesis. To investigate their specific roles in brown fat cells, we generated immortal preadipocyte lines from the brown adipose tissue of mice lacking PGC-1±. We could then efficiently knockdown PGC-1Î² expression by shRNA expression. Loss of PGC-1± did not alter brown fat differentiation but severely reduced the induction of thermogenic genes. Cells deficient in either PGC-1Î± or PGC-1Î² coactivators showed a small decrease in the differentiation-dependant program of mitochondrial biogenesis and respiration; however, this increase in mitochondrial number and function was totally abolished during brown fat differentiation when both PGC-1± and PGC-1 were deficient. These data show that PGC-1± is essential for brown fat thermogenesis but not brown fat differentiation, and the PGC-1 coactivators play an absolutely essential but complementary function in differentiation-induced mitochondrial biogenesis. Affymetrix microarray analysis of total RNA from wt, PGC-1± KO and PGC-1± KO; cells expressing an RNAi specific for PGC-1 knockdown was performed. Of the 461; mitochondrial genes analyzed, 181 were found to be at least 20% different between wt; and defective PGC-1± and Î² adipocytes (p < 0.05). More than 85% of these genes were downregulated in cells deficient for PGC-1alpha and PGC-1beta. Experiment Overall Design: Brown preadipocytes that were either WT, KO for PGC-1alpha, or KO for PGC-1alpha and deficient for PGC-1beta (knockdown through siRNA expression) were differentiated for seven days. RNA was made from biological replicates of the three different types of brown adipocytes (WT, KO expressing a control siRNA, KO expressing a siRNA specific for PGC-1beta knockdown).

2007-11-27 | E-GEOD-5042 | biostudies-arrayexpress

Mus musculus

Project description:Mitochondrial biogenesis induced by PGC-1alpha

| PRJNA94757 | ENA

PGC-1 alpha isoforms and muscle hypertrophy

Project description:An alternative promoter of the PGC-1 alpha gene gives arrise to 3 new isofroms of the PGC-1 alpha gene refered to as PGC-1a2 (A2), PGC-1a3 (A3) and PGC-1a4 (A4). The proximal PGC-1 alpha promotor transcribes the canonical PGC-1 alpha which is refered to as PGC-1a1 (A1).G1/G2/G3 samples refer to the Green fluorescent protein (GFP) control samples used in this experiment. Forced expression of specifically PGC-1a4 isoform results in muslce hypertrophy associated with increased IGF-1 signaling and repression of myostatin signaling. Adnoviral over expression assays were performed on primary myoblasts from C57BL/6 mice for each of the PGC-1 alpha isoforms originating from the proximal or alternative promotor.

2012-12-04 | E-GEOD-42473 | biostudies-arrayexpress

Complementary action of the PGC-1 coactivators in mitochondrial biogenesis and brown fat differentiation

Project description:Mitochondria play an essential role in the ability of brown fat to generate heat, and the PGC-1 coactivators control several aspects of mitochondrial biogenesis. To investigate their specific roles in brown fat cells, we generated immortal preadipocyte lines from the brown adipose tissue of mice lacking PGC-1α. We could then efficiently knockdown PGC-1β expression by shRNA expression. Loss of PGC-1α did not alter brown fat differentiation but severely reduced the induction of thermogenic genes. Cells deficient in either PGC-1α or PGC-1β coactivators showed a small decrease in the differentiation-dependant program of mitochondrial biogenesis and respiration; however, this increase in mitochondrial number and function was totally abolished during brown fat differentiation when both PGC-1α and PGC-1β were deficient. These data show that PGC-1α is essential for brown fat thermogenesis but not brown fat differentiation, and the PGC-1 coactivators play an absolutely essential but complementary function in differentiation-induced mitochondrial biogenesis. Affymetrix microarray analysis of total RNA from wt, PGC-1α KO and PGC-1α KO cells expressing an RNAi specific for PGC-1β knockdown was performed. Of the 461 mitochondrial genes analyzed, 181 were found to be at least 20% different between wt and defective PGC-1α and β adipocytes (p < 0.05). More than 85% of these genes were downregulated in cells deficient for PGC-1alpha and PGC-1beta. Keywords: Analysis of mitochondrial gene expression

2006-07-06 | GSE5042 | GEO

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