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Single cell transcriptomic analysis reveals cellular diversity of murine esophageal epithelium and age-associated mitochondrial dysfunction

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE193377 | GEO | 2022/01/14

REPOSITORIES: GEO

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Single cell transcriptomic analysis reveals cellular diversity of murine esophageal epithelium and age-associated mitochondrial dysfunction.

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Single cell transcriptomic analysis reveals cellular diversity of murine esophageal epithelium and age-associated mitochondrial dysfunction [bulk RNA-seq]

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Single cell transcriptomic analysis reveals cellular diversity of murine esophageal epithelium.

Project description:Although morphologic progression coupled with expression of specific molecular markers has been characterized along the esophageal squamous differentiation gradient, the molecular heterogeneity within cell types along this trajectory has yet to be classified at the single cell level. To address this knowledge gap, we perform single cell RNA-sequencing of 44,679 murine esophageal epithelial, to identify 11 distinct cell populations as well as pathways alterations along the basal-superficial axis and in each individual population. We evaluate the impact of aging upon esophageal epithelial cell populations and demonstrate age-associated mitochondrial dysfunction. We compare single cell transcriptomic profiles in 3D murine organoids and human esophageal biopsies with that of murine esophageal epithelium. Finally, we employ pseudotemporal trajectory analysis to develop a working model of cell fate determination in murine esophageal epithelium. These studies provide comprehensive molecular perspective on the cellular heterogeneity of murine esophageal epithelium in the context of homeostasis and aging.

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Single cell transcriptomic analysis reveals cellular diversity of murine esophageal epithelium and age-associated mitochondrial dysfunction.

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Single cell transcriptomic analysis reveals cellular diversity of murine esophageal epithelium and age-associated mitochondrial dysfunction

Project description:Single cell transcriptomic analysis reveals cellular diversity of murine esophageal epithelium and age-associated mitochondrial dysfunction

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Single cell transcriptomic analysis reveals cellular diversity of murine esophageal epithelium and age-associated mitochondrial dysfunction [scRNA-seq]

Project description:Single cell transcriptomic analysis reveals cellular diversity of murine esophageal epithelium and age-associated mitochondrial dysfunction [scRNA-seq]

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Single cell transcriptomic analysis reveals cellular diversity of murine esophageal epithelium and age-associated mitochondrial dysfunction [bulk RNA-seq]

Project description:Single cell transcriptomic analysis reveals cellular diversity of murine esophageal epithelium and age-associated mitochondrial dysfunction [bulk RNA-seq]

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Age-Associated Mitochondrial Dysfunction Accelerates Atherogenesis.

Project description:Rationale: Aging is one of the strongest risk factors for atherosclerosis. Yet whether aging increases the risk of atherosclerosis independently of chronic hyperlipidemia is not known. Objective: To determine if vascular aging before the induction of hyperlipidemia enhances atherogenesis. Methods and Results: We analyzed the aortas of young and aged normolipidemic wild type, disease-free mice and found that aging led to elevated IL (interleukin)-6 levels and mitochondrial dysfunction, associated with increased mitophagy and the associated protein Parkin. In aortic tissue culture, we found evidence that with aging mitochondrial dysfunction and IL-6 exist in a positive feedback loop. We triggered acute hyperlipidemia in aged and young mice by inducing liver-specific degradation of the LDL (low-density lipoprotein) receptor combined with a 10-week western diet and found that atherogenesis was enhanced in aged wild-type mice. Hyperlipidemia further reduced mitochondrial function and increased the levels of Parkin in the aortas of aged mice but not young mice. Genetic disruption of autophagy in smooth muscle cells of young mice exposed to hyperlipidemia led to increased aortic Parkin and IL-6 levels, impaired mitochondrial function, and enhanced atherogenesis. Importantly, enhancing mitophagy in aged, hyperlipidemic mice via oral administration of spermidine prevented the increase in aortic IL-6 and Parkin, attenuated mitochondrial dysfunction, and reduced atherogenesis. Conclusions: Before hyperlipidemia, aging elevates IL-6 and impairs mitochondrial function within the aorta, associated with enhanced mitophagy and increased Parkin levels. These age-associated changes prime the vasculature to exacerbate atherogenesis upon acute hyperlipidemia. Our work implies that novel therapeutics aimed at improving vascular mitochondrial bioenergetics or reducing inflammation before hyperlipidemia may reduce age-related atherosclerosis.

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