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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Shih-Hwa Chiou

PROVIDER: E-GEOD-19643 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2010-12-01 | GSE19643 | 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

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

Remodeling of Brown and White Adipose Tissue by NT-PGC-1α-Mediated Gene Regulation

Project description:The β-adrenergic receptor signaling pathway is a major component of adaptive thermogenesis in brown and white adipose tissue during cold acclimation. The β-AR activation highly induces transcriptional coactivator PGC-1α and its splice variant N-terminal (NT)-PGC-1α, promoting the transcription program of mitochondrial biogenesis and thermogenesis. In the present study, we evaluated the role of NT-PGC-1α in brown adipocyte energy metabolism by genome-wide profiling of NT-PGC-1α-responsive genes. Canonical pathway analysis revealed that a number of genes upregulated by NT-PGC-1α are highly enriched in mitochondrial pathways including fatty acid transport and β-oxidation, TCA cycle and electron transport system, thus reinforcing the crucial role of NT-PGC-1α in the enhancement of mitochondrial function. Moreover, gene expression profiling of NT-PGC-1α revealed activation of distinct metabolic pathways such as glucose, lipid and nucleotide metabolism and of signaling pathways such as RAR and PPAR-γ/RXRα activation in brown adipocytes. Together, our data strengthen our previous findings that NT-PGC-1α is a key regulator of mitochondrial oxidative metabolism and thermogenesis in brown adipocytes and further suggest that NT-PGC-1α influences a broader spectrum of thermogenic processes to meet cellular needs for adaptive thermogenesis. Two samples from two groups: NT-PGC-1α overexpression and empty vector. There are technical replicates (A and B) for each group. Two RNA samples were pooled for each group.

2015-08-07 | E-GEOD-71774 | biostudies-arrayexpress

Remodeling of Brown and White Adipose Tissue by NT-PGC-1α-Mediated Gene Regulation

2015-08-07 | GSE71774 | GEO

miRNA expression profiles of PRC SiRNA vs scramble transfected XTC.UC1 cells

Project description:PGC-1 related coactivator (PRC) shares structural and functional features with PGC-1{alpha}. It regulates several metabolic pathways and mitochondrial biogenesis. Its specific role in the early programming of cell proliferation suggests a finely regulated crosstalk between the mitochondrial functions and the cell cycle status. To explore the PRC-regulated pathways, we used a cell-line model of mitochondrial-rich tumors, presenting an oxidative metabolism and a specific increase in PRC expression. We looked for the feedback loop exerted by miRNAs on the regulation of PRC-related mitochondiral functions Expression profiles of miRNA at 48h PRC SIRNA treatment compared to scramble in XTC.UC1 cells. In duplicate.

2011-11-22 | E-GEOD-33843 | biostudies-arrayexpress

A map of the PGC-1α- and NT-PGC-1α-regulated transcriptional network in brown adipose tissue [SAGE]

Project description:Transcriptional coactivator PGC-1α and its splice variant NT-PGC-1α play crucial roles in regulating cold-induced thermogenesis in brown adipose tissue (BAT). PGC-1α and NT-PGC-1α are highly induced by cold in BAT and subsequently bind to and coactivate many different transcription factors to regulate expression of genes involved in mitochondrial biogenesis, fatty acid oxidation, respiration and thermogenesis. To identify the complete repertoire of PGC-1α and NT-PGC-1α target genes in BAT, we analyzed genome-wide DNA-binding and gene expression profiles. We find that PGC-1α-/NT-PGC-1α binding broadly associates with cold-mediated transcriptional activation. In addition to their known target genes in mitochondrial biogenesis, fatty acid oxidation, respiration and thermogenesis, PGC-1α and NT-PGC-1α target to a broad spectrum of genes involved in diverse biological pathways including ubiquitin-dependent protein catabolism, ribonucleoprotein complex biosynthesis, phospholipid biosynthesis, angiogenesis, glycogen metabolism, phosphorylation, and autophagy. Our findings expand the number of genes and biological pathways that may be regulated by PGC-1α and NT-PGC-1α and provide further insight into the transcriptional regulatory network in which PGC-1α and NT-PGC-1α coordinate a comprehensive transcriptional response in BAT in response to cold.

2018-05-22 | GSE110055 | GEO

A map of the PGC-1α- and NT-PGC-1α-regulated transcriptional network in brown adipose tissue [ChIP-Seq]

2018-05-22 | GSE110053 | GEO

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

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