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

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

PROVIDER: PRJNA866488 | ENA |

REPOSITORIES: ENA

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Monoamine oxidase-dependent pro-survival signaling in diabetic hearts

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

| PRJNA866484 | ENA

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

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.

2022-09-20 | GSE210611 | GEO

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

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

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

| PRJNA863650 | ENA

Monoamine oxidase-dependent pro-survival signaling in diabetic hearts

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

2022-09-20 | GSE210612 | GEO

Monoamine Oxidase-Dependent Pro-Survival Signaling in Diabetic Hearts Is Mediated by miRNAs.

Project description:Diabetes leads to cardiomyopathy and heart failure, the leading cause of death for diabetic patients. Monoamine oxidase (MAO) inhibition in diabetic cardiomyopathy prevents oxidative stress, mitochondrial and endoplasmic reticulum stress and the development of diastolic dysfunction. However, it is unclear whether, in addition to the direct effects exerted on the 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 streptozotocin-treated mice (model of type 1 diabetes (T1D)), administered with either vehicle or MAOs inhibitor pargyline for 12 weeks. We found that inhibition of MAO activity in T1D hearts leads to profound transcriptomic changes, affecting autophagy and pro-survival pathways activation. MAO activity in T1D hearts increased miR-133a-3p, -193a-3p and -27a-3p expression. These miRNAs 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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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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Effects of clorgyline, a monoamine oxidase A inhibitor, on high grade prostate cancer cells

2010-07-17 | GSE17167 | GEO

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

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

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

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

| PRJNA778245 | ENA