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Role of Adipocyte Na,K-ATPase Oxidant Amplification Loop in Cognitive Decline and Neurodegeneration - Expression profiling in Brain

ABSTRACT: Role of Adipocyte Na,K-ATPase Oxidant Amplification Loop in Cognitive Decline and Neurodegeneration - Expression profiling in Brain

PROVIDER: PRJNA689814 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13361525_1.fastq.gz	Fastqsanger.gz
	SRR13361525_2.fastq.gz	Fastqsanger.gz
	SRR13361526_1.fastq.gz	Fastqsanger.gz
	SRR13361526_2.fastq.gz	Fastqsanger.gz
	SRR13361527_1.fastq.gz	Fastqsanger.gz

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Role of Adipocyte Na,K-ATPase Oxidant Amplification Loop in Cognitive Decline and Neurodegeneration

Project description:Role of Adipocyte Na,K-ATPase Oxidant Amplification Loop in Cognitive Decline and Neurodegeneration

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Role of Adipocyte Na,K-ATPase Oxidant Amplification Loop in Cognitive Decline and Neurodegeneration - Expression profiling in Brain

Project description:Adipocyte-specific expression of Na,K-ATPase signaling antagonist, NaKtide, has been shown to ameliorate the pathophysiological consequences of obesity and improve diseased phenotype. Recent studies have established that the release of adipocytokines and other bioactive mediators in obesity contributes to neurodegeneration. This study utilizes a mechanistic approach and characterizes the hippocampal transcriptome in comparison with transcriptomic changes in liver, visceral and subcutaneous adipose tissue. RNAseq analysis in high fat diet fed transgenic mice showed large scale differential gene expression as well as modulation of several biological pathways in hippocampus, liver, visceral and subcutaneous adipose tissue, which were attenuated by doxycycline induced adipocyte specific NaKtide expression.

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Role of Adipocyte Na,K-ATPase Oxidant Amplification Loop in Cognitive Decline and Neurodegeneration - Expression profiling in Liver and Fat

Project description:Role of Adipocyte Na,K-ATPase Oxidant Amplification Loop in Cognitive Decline and Neurodegeneration - Expression profiling in Liver and Fat

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Oxidant Alterations in Adipocyte mRNA Expression: Role of the Na,K-ATPase Oxidant Amplification Loop

Project description:Oxidant Alterations in Adipocyte mRNA Expression: Role of the Na,K-ATPase Oxidant Amplification Loop

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Role of Adipocyte Na,K-ATPase Oxidant Amplification Loop in Cognitive Decline and Neurodegeneration

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

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Role of adipocyte Na,K-ATPase oxidant amplification loop in cognitive decline and neurodegeneration

Project description:Summary Recent studies suggest that a western diet may contribute to clinical neurodegeneration and dementia. Adipocyte-specific expression of the Na,K-ATPase signaling antagonist, NaKtide, ameliorates the pathophysiological consequences of murine experimental obesity and renal failure. In this study, we found that a western diet produced systemic oxidant stress along with evidence of activation of Na,K-ATPase signaling within both murine brain and peripheral tissues. We also noted this diet caused increases in circulating inflammatory cytokines as well as behavioral, and brain biochemical changes consistent with neurodegeneration. Adipocyte specific NaKtide affected by a doxycycline on/off expression system ameliorated all of these diet effects. These data suggest that a western diet produces cognitive decline and neurodegeneration through augmented Na,K-ATPase signaling and that antagonism of this pathway in adipocytes ameliorates the pathophysiology. If this observation is confirmed in humans, the adipocyte Na,K-ATPase may serve as a clinical target in the therapy of neurodegenerative disorders. Graphical abstract Highlights • Adipocytes induce phenotypical changes in neurodegeneration through adipocyte NKAL• Adipocyte specific NaKtide inhibited NKAL and improved systemic homeostasis• NaKtide improved adipocyte phenotype and improved markers of neurodegeneration• NaKtide improved genomic profile of hippocampus and adipose tissue in WD fed mice Molecular physiology; Neuroscience; Cell biology

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Project description:Exposure to hypoxia requires adaptive mechanisms for survival. During acute hypoxia, Na,K-ATPase endocytosis in alveolar epithelial cells (AEC) occurs via protein kinase C zeta (PKCζ) phosphorylation of α1- Na,K-ATPase independently of the hypoxia inducible factor (HIF). However, exaggerated Na,K-ATPase down-regulation leads to cell death. Here we report that during prolonged hypoxia plasma membrane Na,K-ATPase levels were maintained at ~50% of normoxic values due to HIF mediated regulation of HOIL-1L which targets PKCζ for degradation. Silencing HOIL-1L in the lung epithelium prevented PKCζ degradation causing Na,K-ATPase downregulation. Accordingly, HIF regulation of HOIL-1L targets the phosphorylated PKCζ for degradation and serves as an hypoxia-adaptive mechanism to stabilize the Na,K-ATPase avoiding significant lung injury.

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Project description:Familial hemiplegic migraine is an episodic neurological disorder characterized by transient sensory and motor symptoms and signs. Mutations of the ion pump alpha2-Na/K ATPase represent a key genetic cause of familial hemiplegic migraine, but the mechanisms by which alpha2-Na/K ATPase mutations lead to the migraine phenotype remain incompletely understood. Here, we unexpectedly find that mice in which alpha2-Na/K ATPase is conditionally deleted in astrocytes display episodic transient motor paralysis. Functional neuroimaging reveals that conditional knockout of alpha2-Na/K ATPase triggers spontaneous cortical spreading depression events that are associated with low voltage activity events upon EEG monitoring, which in turn correlate with transient motor impairment in these mice. Transcriptomic and metabolomic analyses show that loss of alpha2-Na/K ATPase alters metabolic gene expression in astrocytes in vivo with consequent elevation of serine and glycine in the brain. Strikingly, feeding alpha2-Na/K ATPase knockout mice a serine- and glycine-free diet reverses the phenotype of transient motor impairment. Together, our findings define a novel metabolic mechanism regulated by astrocytic alpha2-Na/K ATPase that triggers episodic transient motor paralysis in mice, laying the foundation for potential new treatment strategies for patients with familial hemiplegic migraine.

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Project description:Whole hearts from wild-type and Na,K-ATPase alpha 1 het. mice. Adult male, 8-16 weeks old on a 129/BSwiss background. Keywords: repeat sample

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