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Distinct functional programming of human fetal and adult monocytes [set 2]

ABSTRACT: Microarray profiling of unstimulated and IFNg-stimulated human fetal and adult bone marrow classical monocytes

ORGANISM(S): Homo sapiens

PROVIDER: GSE54817 | GEO | 2014/05/02

SECONDARY ACCESSION(S): PRJNA237756

REPOSITORIES: GEO

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Distinct functional programming of human fetal and adult monocytes [set 2]

Project description:Microarray profiling of unstimulated and IFNg-stimulated human fetal and adult bone marrow classical monocytes Classical monocytes were stimulated or no with IFNg for 4 hours, sort purified, RNA isolated, and amplified. 4 of each sample was collected and used

2014-05-02 | E-GEOD-54817 | biostudies-arrayexpress

Distinct functional programming of human fetal and adult monocytes [set 1]

Project description:Microarray profiling of unstimulated human fetal and adult bone marrow classical monocytes

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Distinct functional programming of human fetal and adult monocytes [set 1]

Project description:Microarray profiling of unstimulated human fetal and adult bone marrow classical monocytes Classical monocytes were sort purified, RNA isolated, and amplified. 4 of each sample was collected and used

2014-05-02 | E-GEOD-54668 | biostudies-arrayexpress

Distinct functional programming of human fetal and adult monocytes.

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Project description:Monocytes were isolated from healthy donors PBMC and sorted for classical and non-classical monocyte subsets. RNA-seq was performed on unstimulated monocytes.

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Distinct functional programming of human fetal and adult monocytes

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-05-02 | E-GEOD-54818 | biostudies-arrayexpress

Distinct functional programming of human fetal and adult monocytes

Project description:This SuperSeries is composed of the SubSeries listed below.

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RNA-seq of primary mouse monocytes from miR-150 knockout and Tet3 knockout mice compared to wild type controls

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IFNg treatment of monocytes

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IFNg Regulates NAD+ Metabolism in Human Monocytes

Project description:IFNg is an essential and pleiotropic activator of monocytes, but little is known about the changes in cellular metabolism required for IFNg-induced activation. We sought to characterize and elucidate the mechanisms by which IFNg reprograms monocyte metabolism to support its immunologic activities. Monocytes from healthy controls and patients with gain-of-function mutations in STAT1 (STAT1 GOF), or loss-of-function mutations in mitochondrial complex I (Leigh syndrome) and NADPH oxidase (chronic granulomatous disease, CGD) were metabolically phenotyped. We found that IFNg increased oxygen consumption rates (OCR), indicative of reactive oxygen species generation by both mitochondria and NADPH oxidase. Transcriptional profiling of human monocyte derived macrophages revealed that this oxidative phenotype was driven by an IFNg-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively. Monocytes from patients with STAT1 GOF demonstrated higher than normal OCR, while monocytes from Leigh syndrome and CGD patients demonstrated reduced OCR. Chemical inhibition of NAMPT completely abrogated the IFNg-induced oxygen consumption, comparable to levels observed in CGD patients. These data identify an IFNg-induced, NAMPT-dependent, NAD+ salvage pathway that is critical for IFNg activation of human monocytes.

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