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Autophagy contributes to homeostasis in esophageal epithelium where high autophagic vesicle content marks basal cells with limited proliferation and enchanced self-renewal potential [scRNA-Seq]

ABSTRACT: Autophagy contributes to homeostasis in esophageal epithelium where high autophagic vesicle content marks basal cells with limited proliferation and enchanced self-renewal potential [scRNA-Seq]

PROVIDER: PRJNA1018966 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26113055_1.fastq.gz	Fastqsanger.gz
	SRR26113055_2.fastq.gz	Fastqsanger.gz
	SRR26113056_1.fastq.gz	Fastqsanger.gz
	SRR26113056_2.fastq.gz	Fastqsanger.gz
	SRR26113057_1.fastq.gz	Fastqsanger.gz

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Autophagy contributes to homeostasis in esophageal epithelium where high autophagic vesicle content marks basal cells with limited proliferation and enchanced self-renewal potential [RNA-Seq]

Project description:We used bulk RNA-seq to examine the molecular alterations between esophageal epithelial cells with low and high autophagic vesicle content.

2023-09-20 | GSE243539 | GEO

Autophagy contributes to homeostasis in esophageal epithelium where high autophagic vesicle content marks basal cells with limited proliferation and enchanced self-renewal potential [scRNA-Seq]

Project description:We used scRNA-seq to examine the cellular and molecular alterations between 3D organoids generated from esophageal epithelial cells with low and high autophagic vesicle content.

2023-09-20 | GSE243580 | GEO

Autophagy contributes to homeostasis in esophageal epithelium where high autophagic vesicle content marks basal cells with limited proliferation and enchanced self-renewal potential

Project description:Autophagy contributes to homeostasis in esophageal epithelium where high autophagic vesicle content marks basal cells with limited proliferation and enchanced self-renewal potential

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Autophagy contributes to homeostasis in esophageal epithelium where high autophagic vesicle content marks basal cells with limited proliferation and enchanced self-renewal potential [RNA-Seq]

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High autophagic vesicle content marks facultative stem cells of the gut.

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Autophagy contributes to homeostasis in esophageal epithelium where high autophagic vesicle content marks basal cells with limited proliferation and enchanced self-renewal potential

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

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Autophagy Contributes to Homeostasis in Esophageal Epithelium Where High Autophagic Vesicle Level Marks Basal Cells With Limited Proliferation and Enhanced Self-Renewal Potential.

Project description: Not available

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Profiling of purified autophagic vesicle content and degradome in the maturing and aging brain - Part II

Project description:In this second part of the project “Profiling of purified autophagic vesicle content and degradome in the maturing and aging brain” four label-free proteomics studies were performed to characterize stabilization of potential autophagy targets upon lysosomal and/or autophagy inhibition.

2023-08-07 | PXD041376 | Pride

Autophagic vesicle content profiling from hippocampal slices LC-MSMS

Project description:Previous work demonstrated that the developmental pruning of dendritic spines requires autophagy. This developmental process is facilitated by long-term depression (LTD)-like mechanisms, inviting the speculation that LTD, a fundamental form of plasticity, itself requires autophagy. Here, we show that LTD-inducing activation of NMDA receptors or metabotropic glutamate receptors triggers the rapid initiation of autophagy in postsynaptic dendrites. Dendritic autophagic vesicles (AVs) act in parallel with the endocytic machinery to remove AMPAR subunits from the surface and rapidly degrade them and their scaffold PSD95. Moreover, during NMDAR-LTD, key postsynaptic proteins are sequestered for autophagic degradation, as revealed by quantitative proteomic profiling of purified AVs. In turn, pharmacological inhibition of AV biogenesis, or conditional ablation of atg5 in pyramidal neurons abolishes LTD and instead triggers sustained potentiation in the hippocampus. These deficits in synaptic plasticity are recapitulated by knockdown of atg5 specifically in postsynaptic pyramidal neurons in the CA1 area. Conducive to the role of synaptic plasticity in behavioral flexibility, mice with autophagy deficiency in excitatory neurons exhibit altered response in reversal learning. Therefore, local assembly of the autophagic machinery in dendrites ensures the degradation of postsynaptic components and facilitates LTD expression.

2022-01-10 | PXD030079 | Pride

Colchicine Ameliorates Doxorubicin Cardiotoxicity Via Promoting Autophagic Flux

Project description:Doxorubicin (DOX) cardiotoxicity is an important factor of heart failure. The only clinically approved drug is dexrazoxane, while its side effect of secondary malignancies severely limited its application. It is urgent to find other alternative efficacious molecular for these chemotherapy patients. Colchicine is a safe and well tolerated anti-inflammation drug which also functions in attenuating the reactive oxygen species (ROS) generation. High dose of colchicine was reported block the autophagosome-lysosome fusion in cancer cells due to its destabilization effect to the microtubule system, while how colchicine affects the autophagic flux in cardiomyocytes is largely unknown. Recent years low dose of colchicine administration was reported helpful to the patients with pericarditis, postprocedural atrial fibrillation and coronary artery disease, most of the research attributed it to its anti-inflammation effect. Whether the autophagic flux regulated by colchicine also benefits to DOX induced heart failure remains unclear. Doxorubicin (DOX) administration was used to establish heart failure models in vivo and in vitro. Results showed that DOX blocked the autophagic vacuoles degradation, leading to damaged mitochondria and ROS accumulation. Heart failure characteristics were obviously improved after low dose of colchicine administration. Mechanistically, low dose of colchicine promoted the autolysosome degradation, cleared the damaged mitochondria, and ROS accumulation induced by the DOX and as a result attenuated DOX cardiotoxicity.

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