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Cell-specific proteome analyses of human bone marrow reveal molecular features of age-dependent functional decline

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE115353 | GEO | 2018/07/19

REPOSITORIES: GEO

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Cell-specific proteome analyses of human bone marrow reveal molecular features of age-dependent functional decline.

Project description: Not available

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Cell-specific proteome analyses of human bone marrow reveal molecular features of age-dependent functional decline [single cells]

Project description:Diminishing potential to replace damaged tissues is a hallmark for ageing of somatic stem cells, but the mechanisms leading to ageing remain elusive. We present a proteome-wide atlas of age-associated alterations in human haematopoietic stem and progenitor cells (HPCs) along with five other cell types that constitute the bone marrow niche. For each, the abundance of a large fraction of the ~12,000 proteins identified was assessed in a cohort of healthy human subjects from different age. As the HPCs became older, pathways in central carbon metabolism exhibited features reminiscent of the Warburg effect where glycolytic intermediates are rerouted towards anabolism. Simultaneously, altered abundance of early regulators of HPC differentiation revealed a reduced functionality and a bias towards myeloid differentiation at the expense of lymphoid development. Ageing caused significant alterations in the bone marrow niche too, such as functionality of the pathways involved in HPC homing and lineage differentiation. The data represents a valuable resource for further in-depth mechanistic analyses, and for validation of knowledge gained from animal models.

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Cell-specific proteome analyses of human bone marrow reveal molecular features of age-dependent functional decline [cell populations]

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Cell-specific proteome analyses of human bone marrow reveal molecular features of age-dependent functional decline

Project description:Cell-specific proteome analyses of human bone marrow reveal molecular features of age-dependent functional decline

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Cell-specific proteome analyses of human bone marrow reveal molecular features of age-dependent functional decline [single cells]

Project description:Cell-specific proteome analyses of human bone marrow reveal molecular features of age-dependent functional decline [single cells]

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Transcriptome and Proteome Mapping in the Sheep Atria Reveal Molecular Features of Atrial Fibrillation Progression

Project description:Atrial fibrillation (AF) is often a progressive cardiac arrhythmia that increases the risk of hospitalization and adverse cardiovascular events. There is a clear demand for more inclusive and large-scale approaches to understand the molecular drivers responsible for AF, as well as the fundamental mechanisms governing the transition from paroxysmal to persistent and permanent forms. We aimed to create a molecular map of AF and find the distinct genetic programs underlying cell type-specific atrial remodeling and AF progression. We used a sheep model of long-standing, tachypacing-induced AF, sampled right and left atrial tissue and isolated cardiomyocytes from control, intermediate (transition) and late time points during AF progression, and performed transcriptomic and proteome profiling. We have merged all these layers of information into a meaningful 3-component space in which we explored the genes and proteins detected and their common patterns of expression. Our data-driven analysis points at extracellular matrix remodeling, inflammation, ion channel, myofibril structure, mitochondrial complexes and chromatin remodeling as hallmarks of AF progression. Most important, we prove that these changes occur at early transitional stages of the disease, but not at later stages, and that the left atrium undergoes significantly more profound changes than the right atrium in its expression program. The pattern of dynamic changes in gene and protein expression correspond closely with the electrical and structural remodeling demonstrated previously in the sheep and in humans. The results provide novel insight into the dynamics of gene and protein expression changes that underlie AF-induced atrial remodeling and that make the arrhythmia become more stable and long lasting.

2020-09-30 | GSE138255 | GEO

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