IlCneStep
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB79704 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR13654236_1.fastq.gz | Fastqsanger.gz | |||
| ERR13654236_2.fastq.gz | Fastqsanger.gz | |||
| ERR13650039.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
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Project description:Cnephasia stephensiana (grey tortrix), genomic and transcriptomic data
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Project description:Transcriptome profiling reveals different expression pattern in baseline group(after isolated hair follicles---HFs,collect samples immediately), 0G group(sham irradiation, collect organ-cultured HFs for 3 days),and 5G group(5G dose irradiation, collect organ-cultured HFs for 3 days) in ex vivo organ-cultured HFs. Hair greying or canities is one of the earliest phenomena in aging. A worldwide survey based on a large sample of human subjects showed that men grey faster than women, but in distinct scalp regions, and the populations of Asian and African descent had less grey hair than those of the same age of Caucasian descent. The average grey hair age of whites is 34 ± 9.6 years in Caucasians, while 43.9 ± 10.3 years in African. And then clinical observation demonstrates that by the age of 50 in 50% of all men in senile canities, 50% of all hair follicles (HFs) have lost their pigment. In addition, an increasing number of studies found that hair greying acts as an important predictor of aging-associated pathology, including Alzheimer’s disease, Parkinson’s disease and cardiovascular disease, etc. Grey hair is both visible and non-lethal, and it makes this phenotype a unique model system for investigating mechanisms that contribute to tissue aging and therapeutic strategies to combat this process. In humans and mice, age-related grey hair is attributed to the loss of melanocyte stem cells (MeSCs), precursor cells, and melanocytes, or their reduced or restricted functions, which is induced by a multitude of exogenous and endogenous challenges, such as radiation, inflammation, psycho-emotional stress, or gene mutation (BCL-2 deficiency), etc. Of which, ionizing radiation (IR) produces multiple clusters of double-strand breaks that mediate cell cycle arrest, apoptosis, and DNA repair, and successfully induces grey hair in mice. The accelerating process of aging by IR may provide an avenue to create a grey hair model. Although there is a mouse model of grey hair, the existence of species differences also limits the translational potential of the mice HF models for human applications. Recently, Rachmin et al demonstrated that IR could result to ectopically pigmented melanocytes (EPM) in outer root sheath (ORS) followed hair greying and speculated that this may provide a tool to prevent or reverse hair greying in humans. They proved that different genotoxicity can induce premature differentiation of MeSCs and/or amelanotic cells. However, they didn’t determine the appropriate dose of irradiation for creating the hair grey model and not discuss the mechanisms of forming the model. Hence, this study focuses on establishing a suitable ex vivo human grey HF model by IR, demonstrating the series change of grey hair and exploring the possible mechanisms of the model. In our study, parameters about senescence and melanotic features in our model are almost in line with essential traits of human grey hair in previous studies. In addition,to explore the profound mechanism of the irradiated model, we performed transcriptome analysis for baseline, 0G and 5G groups. Then, three pairwise comparisons were established---0G vs 5G, baseline vs 5G and baseline vs 0G. This profiling results be used to understand the different molecular mechanism of creating ex vivo grey HFs model,and those provided a possibility for anti-aging treatment.In summary, our results indicate that the ex vivo grey HFs by irradiation can perfectly replace elderly grey hair and establish a potential preclinical aging model for pharmacological and mechanism studies.
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Project description:Increasing evidence indicates heterogeneity in functional and molecular properties of oligodendrocyte lineage cells both during development and under pathologic conditions. In multiple sclerosis, remyelination of grey matter lesions exceeds that in white matter. Here we used cells derived from grey matter versus white matter regions of surgically resected human brain tissue samples, to compare the capacities of human A2B5-positive progenitor cells and mature oligodendrocytes to ensheath synthetic nanofibers, and relate differences to the molecular profiles of these cells. For both cell types, the percentage of ensheathing cells was greater for grey matter versus white matter cells. For both grey matter and white matter samples, the percentage of cells ensheathing nanofibers was greater for A2B5-positive cells versus mature oligodendrocytes. Grey matter A2B5-positive cells were more susceptible than white matter A2B5-positive cells to injury induced by metabolic insults. Bulk RNA sequencing indicated that separation by cell type (A2B5-positive vs mature oligodendrocytes) is more significant than by region but segregation for each cell type by region is apparent. Molecular features of grey matter versus white matter derived A2B5-positive and mature oligodendrocytes were lower expression of mature oligodendrocyte genes and increased expression of early oligodendrocyte lineage genes. Genes and pathways with increased expression in grey matter derived cells with relevance for myelination included those related to responses to external environment, cell-cell communication, cell migration, and cell adhesion. Immune and cell death related genes were up-regulated in grey matter derived cells. We observed a significant number of up-regulated genes shared between the stress/injury and myelination processes, providing a basis for these features. In contrast to oligodendrocyte lineage cells, no functional or molecular heterogeneity was detected in microglia maintained in vitro, likely reflecting the plasticity of these cells ex vivo. The combined functional and molecular data indicate that grey matter human oligodendrocytes have increased intrinsic capacity to myelinate but also increased injury susceptibility, in part reflecting their being at a stage earlier in the oligodendrocyte lineage.
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