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A Neurogenic Signature Involving Monoamine Oxidase-A Controls Human Thermogenic Adipose Tissue Development

ABSTRACT: A Neurogenic Signature Involving Monoamine Oxidase-A Controls Human Thermogenic Adipose Tissue Development

PROVIDER: PRJNA823047 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18604226.fastq.gz	Fastqsanger.gz
	SRR18604227.fastq.gz	Fastqsanger.gz
	SRR18604228.fastq.gz	Fastqsanger.gz
	SRR18604229.fastq.gz	Fastqsanger.gz
	SRR18604230.fastq.gz	Fastqsanger.gz

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A Neurogenic Signature Involving Monoamine Oxidase-A Controls Human Thermogenic Adipose Tissue Development

Project description:Mechanisms that control “beige/brite” thermogenic adipose tissue development may be harnessed to improve human metabolic health. To define these mechanisms, we developed a species-hybrid model in which human mesenchymal progenitor cells were used to develop white or thermogenic/beige adipose tissue in mice. The hybrid adipose tissue developed distinctive features of human adipose tissue, such as larger adipocyte size, despite its neurovascular architecture being entirely of murine origin. Thermogenic adipose tissue recruited a denser, qualitatively distinct vascular network, differing in genes mapping to circadian rhythm pathways, and denser sympathetic innervation. The enhanced thermogenic neurovascular network was associated with human adipocyte expression of THBS4, TNC, NTRK3 and SPARCL1, which enhance neurogenesis, and decreased expression of MAOA and ACHE, which control neurotransmitter tone. Systemic inhibition of MAOA, which is present in human but absent in mouse adipocytes, induced browning of human but not mouse adipose tissue, revealing the physiological relevance of this pathway. Our results reveal species-specific cell type dependencies controlling the development of thermogenic adipose tissue and point to human adipocyte MAOA as a potential target for metabolic disease therapy.

2022-09-27 | GSE200141 | GEO

A neurogenic signature involving monoamine Oxidase-A controls human thermogenic adipose tissue development.

Project description:Mechanisms that control 'beige/brite' thermogenic adipose tissue development may be harnessed to improve human metabolic health. To define these mechanisms, we developed a species-hybrid model in which human mesenchymal progenitor cells were used to develop white or thermogenic/beige adipose tissue in mice. The hybrid adipose tissue developed distinctive features of human adipose tissue, such as larger adipocyte size, despite its neurovascular architecture being entirely of murine origin. Thermogenic adipose tissue recruited a denser, qualitatively distinct vascular network, differing in genes mapping to circadian rhythm pathways, and denser sympathetic innervation. The enhanced thermogenic neurovascular network was associated with human adipocyte expression of THBS4, TNC, NTRK3, and SPARCL1, which enhance neurogenesis, and decreased expression of MAOA and ACHE, which control neurotransmitter tone. Systemic inhibition of MAOA, which is present in human but absent in mouse adipocytes, induced browning of human but not mouse adipose tissue, revealing the physiological relevance of this pathway. Our results reveal species-specific cell type dependencies controlling the development of thermogenic adipose tissue and point to human adipocyte MAOA as a potential target for metabolic disease therapy.

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Monoamine oxidase-dependent pro-survival signaling in diabetic hearts

Project description:Monoamine oxidase-dependent pro-survival signaling in diabetic hearts

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Effects of clorgyline, a monoamine oxidase A inhibitor, on high grade prostate cancer cells

Project description:Monoamine oxidase A (MAO-A), a mitochondrial enzyme that degrades monoamines including neurotransmitters, is highly expressed in basal cells of the normal human prostatic epithelium and in poorly differentiated (Gleason grades 4 and 5), aggressive prostate cancer (PCa). Clorgyline, an MAO-A inhibitor, induces secretory differentiation of normal prostate cells. We systematically assessed gene expression changes induced by clorgyline in E-CA cells using high-density oligonucleotide microarrays. Genes differentially expressed in treated and control cells were identified by Significance Analysis of Microarrays. Expression of genes of interest was validated by quantitative real-time polymerase chain reaction. time series design

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Monoamine oxidase-dependent pro-survival signaling in diabetic hearts [total RNA]

Project description:Monoamine oxidase-dependent pro-survival signaling in diabetic hearts [total RNA]

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Monoamine oxidase-dependent pro-survival signaling in diabetic hearts is mediated by miRNAs

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Project description:Diabetes leads to cardiomyopathy and heart failure, the leading cause of death for diabetic patients. Monoamine oxidase (MAO)-dependent reactive oxygen species (ROS) formation contributes to the development of diabetic cardiomyopathy by inducing mitochondrial and cardiomyocyte dysfunction. Yet, it is unclear whether, in addition to the direct effects exerted by MAO-dependent ROS on mitochondria, MAO activity is able to post-transcriptionally regulate cardiomyocyte function and survival in diabetes. To this aim, we performed gene and miRNA expression profiling in cardiac tissue from a mouse model of type 1 diabetes (T1D) with or without pharmacological MAO inhibition. We found that MAO-dependent ROS generation in T1D hearts leads to profound transcriptomic changes, affecting autophagy and pro-survival pathways activation. MAO activity in T1D hearts affected expression levels of miR-133a-3p, -193a-3p, and -27a-3p that target insulin-like growth factor receptor 1 (Igf1r), growth factor receptor bound protein 10 and inositol polyphosphate 4 phosphatase type 1A, respectively, all components of the Igf1r/PI3K/Akt signaling pathway. Indeed, Akt activation was significantly downregulated in T1D hearts, whereas MAO inhibition restored the activation of this pro-survival pathway. The present study provides an important link between MAO activity, transcriptomic changes, and activation of pro-survival signaling and autophagy in diabetic cardiomyopathy.

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Project description:Transcriptional analysis of the effect of monoamine oxidase B (MAOB) in human prostate stromal cells (PrSC)

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