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Endothelial UCP2 regulates the neurogenic-to-astrogenic fate switch during brain development

ABSTRACT: Endothelial UCP2 regulates the neurogenic-to-astrogenic fate switch during brain development

PROVIDER: PRJNA770299 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16295317_1.fastq.gz	Fastqsanger.gz
	SRR16295317_2.fastq.gz	Fastqsanger.gz
	SRR16295318_1.fastq.gz	Fastqsanger.gz
	SRR16295318_2.fastq.gz	Fastqsanger.gz
	SRR16295319_1.fastq.gz	Fastqsanger.gz

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Endothelial UCP2 regulates the neurogenic-to-astrogenic fate switch during brain development

Project description:Purpose: To gain futher insight into how endothelial UCP2 regulates the neurogenic-to-astrogenic fate switch ,RNA-seq was used to analyze the genome-wide changes resulting from isolated endothelial cells of E14.5 and E17.5 UCP2 endothelial conditional knock out mice and littermate wild-type. Methods: mRNA from E15 and E18 isolated endothelial cells of wild-type(WT) and UCP2f/f;Tie2-cre mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, mRNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics Results: Approximately one thousand transcripts showed differential expression between the wild-type(WT) and UCP2ECKO mice brain cortex, with a fold change ≥2 and p value <0.05.Geneontology analysis of the up-regulated genes showed obvious enrichment of biological processes related to development process and regulation of cell communication.The down-regulated genes exhibited enrichment of biological processes related to cell fate commitment. These results reflected endothelial UCP2 plays roles in cortex development. Conclusions: Endothelial UCP2 RNA-seq would provide a overall understanding how endothelial UCP2 regulates the neurogenic-to-astrogenic fate switch during brain development

2021-10-13 | GSE185656 | GEO

Endothelial Cells Mediated by UCP2 Control the Neurogenic-to-Astrogenic Neural Stem Cells Fate Switch During Brain Development.

Project description: Not available

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Expression data in Ucp2+/+ (WT) and Ucp2-/- (KO) colon tumors from AOM/DSS-treated mice

Project description:The objective of the study was to evalute the changes in gene expression associated to UCP2 invalidation in colon tumors from AOM/DSS-treated mice We used microarrays (Mouse Gene 2.0) to investigate gene expression in Ucp2+/+ and Ucp2-/- colon tumors

2019-08-27 | GSE104403 | GEO

RNA-seq of mouse Pmel-1 CD8 T cell with Ucp2 inhibition and NAC treatment

Project description:Enhanced T cell stemness and anti-tumor activity of adoptively transferred T cells are linked to T cell metabolism, however, the mitochondrial regulation of T-cell longevity and anti-tumor activity remains elusive. Here, using loss and gain of function experiments, we show that a mitochondrial inner membrane protein, Uncoupling protein 2 (Ucp2), is required for T cell longevity and anti-tumor function. Loss of mitochondrial Ucp2 activity in T cells results in accelerated differentiation into ‘terminal effector cells’. We found that Ucp2 modulate oxidative stress and DNA damage by regulating the levels of mitochondrial superoxide. We observed that reducing mitochondrial ROS was sufficient to rescue the loss of Ucp2-mediated increase in effector T cell differentiation, senescence, cytokine production and anti-tumor activity. Tumor-specific CD8+ T cells could be metabolically reprogrammed by increasing Ucp2 levels and Ucp2-overexpressing T cells displayed long-term survival and restricted tumor growth and prolonged the survival of melanoma-bearing mice. Our results establish a novel role of Ucp2 in regulating T cell longevity and anti-tumor activity by repressing mitochondrial dysfunction and suggest that manipulating Ucp2 levels in T cells should enhance T cell-based immunotherapies for cancer.

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Suppression of UCP2 alleviates leukemogenesis by enhancing branched amino acids induced oxidative stress via activating PI3K/AKT/mTOR signaling

Project description:Although the cellular role of uncoupling protein 2 (UCP2) in tumorigenesis have been reported in various solid tumor models, its role in leukemogenesis remain elusive. Here, we demonstrated that UCP2 was highly expressed in AML, and it is significantly associated with chemoresistance and poor prognosis suggesting that UCP2 can be a potential biomarker for AML treatment. Mechanically, in vitro and in vivo silencing of UCP2 significantly impairs AML cell growth, survival and accompanied with the disruption of mitochondria homeostasis. Interestingly, RNA-seq analysis and metabolic mass spectrometry revealed that silencing UCP2 results in accumulation of branched chain amino acids (BCAA), which in turn induced oxidative stress through activating PI3K/AKT and mTOR signaling pathway. Additionally, lack of BCAA restored leukemic cell growth, cell survival and decreased mitochondria ROS production which is induced by inhibiting UCP2. Notably, supplementation of BCAA enhanced anti-tumor activity of Genipin, a selective inhibitor that targets UCP2, results in significant reduction of AML blasts, increased mice survival and magnified oxidative stress. Taken together, our study elucidates the rationale of targeting UCP2-BCAA-PI3K/AKT/mTOR signaling axis in leukemogenesis and provide a novel strategy for leveraging the metabolic dependencies of leukemic cells.

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Hdac3 Interaction with p300 Histone Acetyltransferase Regulates the Oligodendrocyte and Astrocyte Lineage Fate Switch (ChIP-Seq)

Project description:Establishment and maintenance of CNS glial cell identity ensures proper brain development and function, yet the epigenetic mechanisms underlying glial fate control remain poorly understood. Here we show that the histone deacetylase Hdac3 controls oligodendrocyte-specification gene Olig2 expression, and functions as a molecular switch for oligodendrocyte and astrocyte lineage determination. Our data suggest that Hdac3 cooperates with p300 to prime and maintain oligodendrogenic programs while inhibiting Stat3-mediated astrogliogenesis, and thereby regulate phenotypic commitment at the point of oligodendrocyte-astrocytic fate decision. Examination of Hdac3 and p300 genomewide occupancy in differentiating oligodendrocytes

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