Comparative transcriptome analysis of dedifferentiation in mouse mature adipocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE156495 | GEO | 2020/09/22
REPOSITORIES: GEO
Similar Datasets
Project description:Cellular dedifferentiation signifies the withdrawal of cells from a specific differentiated state into a M-bM-^@M-^Xstem cellM-bM-^@M-^Y-like undifferentiated state. However, the mechanism of dedifferentiation remains obscure. We showed that mature adipocytes (MA) and follicular granulosa cells (GC), which have distinct functions in vivo, can dedifferentiate during culture in vitro and acquire multipotency. We investigated the dedifferentiation mechanism of MA and GC using global gene expression analyses. Using Affymetrix porcine genome array, we compared global gene expression profiles during dedifferentiation to search for particular biological functions in genes of which expression intensities were increased or decreased by MA and GC dedifferentiation.
2011-03-10 | E-GEOD-17264 | biostudies-arrayexpress
Project description:Cellular dedifferentiation signifies the withdrawal of cells from a specific differentiated state into a ‘stem cell’-like undifferentiated state. However, the mechanism of dedifferentiation remains obscure. We showed that mature adipocytes (MA) and follicular granulosa cells (GC), which have distinct functions in vivo, can dedifferentiate during culture in vitro and acquire multipotency. We investigated the dedifferentiation mechanism of MA and GC using global gene expression analyses.
2011-03-10 | GSE17264 | GEO
Project description:Cellular dedifferentiation signifies the withdrawal of cells from a specific differentiated state into a ‘stem cell’-like undifferentiated state. However, the mechanism of dedifferentiation remains obscure. We showed that follicular granulosa cells (GC), which have distinct functions in vivo, can dedifferentiate during culture in vitro and acquire multipotency. We investigated the dedifferentiation of GC using global gene expression analyses.
2012-11-21 | GSE18854 | GEO
Project description:Cellular dedifferentiation signifies the withdrawal of cells from a specific differentiated state into a M-bM-^@M-^Xstem cellM-bM-^@M-^Y-like undifferentiated state. However, the mechanism of dedifferentiation remains obscure. We showed that follicular granulosa cells (GC), which have distinct functions in vivo, can dedifferentiate during culture in vitro and acquire multipotency. We investigated the dedifferentiation of GC using global gene expression analyses. Total RNA was isolated from GCs to DFOG cells at 5 time points during dedifferentiation (cultured in 0day, 1day, 2day, 4day and 7day). Each timepoint was performed in triplicate (ie, biological replicates). Using Affymetrix porcine genome array, we performed microarray time course experiments to analyze gene expression profiles during GC dedifferentiation.
2012-11-21 | E-GEOD-18854 | biostudies-arrayexpress
Project description:Dedifferentiation is an important process to replenish lost stem cells during aging or regeneration after injury to maintain tissue homeostasis. Here we report that Enhancer of Zeste [E(z)], a component of the Polycomb Repression Complex 2 (PRC2), is required for the partially differentiated germ cell to dedifferentiate, in order to maintain a stable pool of germline stem cells (GSCs) within the niche microenvironment. During aging, germ cells with reduced E(z) activity have defects in maintaining GSCs, which is not due to increased GSC death or premature differentiation. We found evidence that the decrease of GSCs upon inactivation of E(z) in the germline is likely attributed by defective dedifferentiation. In addition, E(z) mutant germ cells fail to replenish lost GSCs during recovery from genetically manipulated GSC depletion. Together, our data suggest that E(z) acts intrinsically in germ cells for the dedifferentiation process to replenish lost GSCs during both aging and tissue regeneration.
2017-05-15 | GSE98000 | GEO
Project description:To investigate the molecular basis of senescence-induced dedifferentiation, we performed RNAseq on control proliferating cells (DMSO only) and etoposide-induced senescent cells to profile senescence induction. Additionally, we performed RNAseq on purified populations of differentiated myotubes derived from untreated A1 cells to investigate differentiation, as well as myotubes subsequently induced to dedifferentiate, either by serum exposure (10% FCS) or by exposure to 48 hour conditioned media from senescent cells (including proliferating cell conditioned media controls). We then performed gene expression profiling analysis using data obtained from RNA-seq of all 6 populations in triplicate.
2023-06-21 | GSE211798 | GEO
Project description:Objective: When primary chondrocytes are cultured in monolayer, they undergo dedifferentiation during which they lose their phenotype and their capacity to form cartilage. Dedifferentiation is an obstacle for cell therapy for cartilage degeneration. In this study, we aimed to systemically evaluate the changes in gene expression during dedifferentiation of human articular chondrocytes to identify underlying mechanisms. Methods: RNA was isolated from monolayer-cultured primary human articular chondrocytes at serial passages. Gene expression was analyzed by microarray. Based on the microarray analysis, relevant genes and pathways were identified. Their functions in chondrocyte dedifferentiation were further investigated in detail. Results: In vitro expanded human chondrocytes showed progressive changes in gene expression during dedifferentiation. Strikingly, an overall decrease in total gene expression was detected. Genes in the Wnt and BMP pathways exhibited significant changes in expression. The non-canonical rather than the canonical Wnt pathway was found to be involved in the loss of collagen II synthesis. BMP2 was able to decelerate the dedifferentiation and reinforce the maintenance of chondrocyte phenotype in monolayer culture. DNA methylation was in part responsible for the expression downregulation of a set of genes. Conclusion: Our study revealed the roles of ERK, Wnt and BMP pathways as well as DNA methylation in chondrocyte dedifferentiation in monolayer culture. RNA human chondrocytes were allowed to dedifferentiate for 8 passages. RNA was isolated at week 0, 2 ,4, 6 and 8, which was subjected to whole genome gene expression analysis.
2012-11-14 | E-GEOD-42235 | biostudies-arrayexpress
Project description:Plant development is characterised by the capacity to reprogram differentiated cells to initiate asexual reproduction and to produce new organs such as lateral roots. To test whether HIRA could be involved in aspects of developmental reprogramming we studied the effect of HIRA during de-differentiation Arabidopsis root tissue was digested with enzyme to generate protoplast. This process would induce plant cell dedifferentiation. Experiments were performed in WT and hira background to understand how hira affect plant dedifferentiation process.
2014-10-01 | E-GEOD-57044 | biostudies-arrayexpress
Project description:Bone marrow mesenchymal stem cells (MSC) were adipogenically differentiated followed by dedifferentiation. We are interested to know the new fat markers, adipogenic signaling pathways and dedifferentiation signaling pathways.Furthermore we are also intrested to know that how differentiated cells convert into dedifferentiated progenitor cells. To address these questions, MSC were adipogenically differentiated, followed by dedifferentiation. Finally these dedifferentiated cells were used for adipogenesis, osteogenesis and chondrogenesis. Histology, FACS, qPCR and GeneChip analyses of undifferentiated, adipogenically differentiated and dedifferentiated cells were performed. Regarding the conversion of adipogenically differentiated cells into dedifferentiated cells, gene profiling and bioinformatics demonstrated that upregulation (DHCR24, G0S2, MAP2K6, SESN3) and downregulation (DST, KAT2, MLL5, RB1, SMAD3, ZAK) of distinct genes play a curcial role in cell cycle to drive the adipogenically differentiated cells towards an arrested state to narrow down the lineage potency. However, the upregulation (CCND1, CHEK, HGF, HMGA2, SMAD3) and downregulation (CCPG1, RASSF4, RGS2) of these cell cycle genes motivates dedifferentiation of adipogenically differentiated cells to reverse the arrested state. We also found new fat markers along with signaling pathways for adipogenically differentiated and dedifferentiated cells, and also observed the influencing role of proliferation associated genes in cell cycle arrest and progression. We have differentiated bone marrow derived mesenchymal stem cells(MSC) into adipogenically differentiated cells followed by dedifferentiation. We are intrested to know new fat markers, signaling pathways for adipogenically differentiated and dedifferentiated cells, along to observe the genes associated with cell cycle arrest and progression. Results are also provide molecular insight into the process of adipogenesis and dedifferentiation. To study the adipogenic differentiation and dedifferentiation process along with "how adipogenically differentiated cells convert into dedifferentiated cells" on the molecular level, gene expression profiling with genome-wide Affymetrix HG-U133 Plus 2.0 olgonucleotide microarrays (Affymetrix, Santa Clara, CA, USA) was applied. In total, 12 GeneChips were performed for n=3 donors and 4 times (3x4=12): 3x P4 MSC (undifferentiated state), 3x adipogenically differentiated cells at day 15 (differentiated state), 3x dedifferentiated cells at day 7 (dedifferentiated state) and 3x dedifferentiated cells at day 35 (dedifferentiated state)
2014-03-29 | E-GEOD-36923 | biostudies-arrayexpress
Project description:Loss of mature β cell function and identity, or β cell dedifferentiation, is seen in all types of diabetes mellitus. Two competing models explain β cell dedifferentiation in diabetes. In the first model, β cells dedifferentiate in the reverse order of their developmental ontogeny. This model predicts that dedifferentiated β cells resemble β cell progenitors. In the second model, β cell dedifferentiation depends on the type of diabetogenic stress. This model, which we call the “Anna Karenina” model, predicts that in each type of diabetes, β cells dedifferentiate in their own way, depending on how their mature identity is disrupted by any particular diabetogenic stress. We directly tested the two models using a β cell-specific lineage-tracing system coupled with RNA-sequencing in mice. We constructed a multidimensional map of β cell transcriptional trajectories during the normal course of β cell postnatal development, and during their dedifferentiation in models of both type 1 diabetes (NOD) and type 2 diabetes (BTBR-Lepob/ob). Using this unbiased approach, we show here that despite some similarities between immature and dedifferentiated β cells, β cells dedifferentiation in the two mouse models is not a reversal of developmental ontogeny and is different between different types of diabetes.
2021-03-12 | GSE168743 | GEO