Single cell RNA-seq of a laser treated alopecia model
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA783893 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17045033_1.fastq.gz | Fastqsanger.gz | |||
| SRR17045033_2.fastq.gz | Fastqsanger.gz | |||
| SRR17045034_1.fastq.gz | Fastqsanger.gz | |||
| SRR17045034_2.fastq.gz | Fastqsanger.gz | |||
| SRR17045035_1.fastq.gz | Fastqsanger.gz |
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Project description:Hair loss, including alopecia, is one of the most common dermatological issues worldwide. At present, the application of fractional CO2 laser in the treatment of alopecia has been few documented, however, the results are varied between the reports. These different results may come from limited knowledge of cellular action in the laser irradiated skin. The objective of this study was to investigate the molecular and cellular mechanism of laser treatment at the affective condition for hair cycle initiation.
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Project description:Two patients with alopecia areata were treated with systemic ruxolitinib. Skin biopsies were taken before starting treatment and 12 weeks after starting treatment. We used microarrays to assess changes in gene expression of affected skin before and after starting treatment Two patients with alopecia areata were recruited for our study. Skin biopsies of affected scalp were taken prior to starting treatment with oral ruxolinitib. Additional skin biopsies were taken 12 weeks after starting treatment. Scalp skin biopsies were taken from patients without alopecia areata for comparison. RNA was extracted, cDNA libraries were made and profiled on affymetrix microarray chips.
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Project description:Autoimmune alopecia is a prevalent, highly morbid disease. The inflammatory pathways causing hair loss are not well characterized. We profiled two tissue microarrays comparing healthy skin to scarring alopecia and alopecia areata via spatial transcriptomics to analyze the genes and pathways dysregulated in autoimmune alopecia in direct proximity to the hair follicle.
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Project description:The Hos: HR-1 mouse strain (HR-1) is an autosomal resessive mutant strain which is widely used in pharmacological and dermatological studies in Japan. Although HR-1 mice have been believed to be Hr gene mutants based on their distinctive alopecia phenotype, there are no reports on either the genetic nature of the Hr gene or mechanism of alopecia. The present study clarified that the HR-1 mice carry a C to T transition in the Hr gene, which causes a proline to serin amino acid change in the functional domain of translated HR protein. It is well known that HR plays an important role in hair follicle regression, and loss of HR function triggers distinctive alopecia with the presence of premature apoptosis in the regressing hair follicle. However, the detailed function of HR protein is still uncertain. To clarify the mechanism by which HR dysfunction causes hair loss, here we performed microarray analysis on the mRNA samples obtained from the regressing hair follicles of the homozygous (HrHos / HrHos) and heterozygous (+/HrHos, control) Hr mutant mice using laser capture microdissection. Our results showed increased expression of apoptosis-related and cell-cycle-repressive genes and decreased expression of cell-cycle-promoting genes, suggesting inhibition of the cell cycle at G0/G1. These findings strongly suggest that the loss of HR function leads to high expression of cell cycle inhibitors, resulting in the hair loss with premature apoptosis in the hair matrix. Experiment Overall Design: Homozygous (HrHos / HrHos) and heterozygous (+/HrHos) Hr mutant mice of the same N1 littermates obtained from a male Hos: HR-1 mouse and a female heterozygous F1 offspring (+/HrHos) between an HR-1 mouse and an ICR mouse were used at day 14 postpartum. +/HrHos mice were used as controls because the Hr gene mutantion is autosomal recessive and the morphological appearance of +/HrHos is as same as that of wild-type mice. Four samples (two from +/HrHos and two from HrHos / HrHos) were analyzed. All RNA samples were extracted from hair follicles of dorsal skin using Laser capture microdissection.
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Project description:Our goal was to develop a transcriptomic description of affected alopecic scalp skin from patients with alopecia areata.
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