Vitiligo non-responding lesions to narrow band UVB have intriguing cellular and molecular abnormalities that may prevent epidermal repigmentation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1078844 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28034541.fastq.gz | Fastqsanger.gz | |||
| SRR28034542.fastq.gz | Fastqsanger.gz | |||
| SRR28034543.fastq.gz | Fastqsanger.gz | |||
| SRR28034544.fastq.gz | Fastqsanger.gz | |||
| SRR28034545.fastq.gz | Fastqsanger.gz |
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Project description:We have discovered that human vitiligo patients treated with narrow-band UVB (NBUVB) demonstrated localized resistance to repigmentation in skin sites characterized by distinct cellular and molecular pathways. We used the remaining slides from our immunostaining studies. 1.0 mm2 epidermal scrapes were collected from formalin fixed paraffin embedded (FFPE) transverse sections of biopsies from four paired responding and non-responding vitiligo lesions (8 samples total), following published work (Trejo et al., 2019; Yeakley). The material collected was subjected to whole transcriptome TempO-Seq assay. We used a novel method that combines epidermal scraping and TempO-Seq transcriptome analysis and found that the abnormal environment in non-responding was driven by dysregulated cAMP and WNT/β-catenin signaling pathways. Characterization of abnormal environment that prevents vitiligo repigmentation may open roads for discovery of new drugs that reverse depigmentation.
2024-02-27 | GSE256271 | GEO
Project description:We sought to define the cutaneous response at 24 hours following erythemogenic doses of narrow-band UVB (NB-UVB, 312 nm peak) exposure and determine the differences between irradiated and non-irradiated skin.
2012-10-30 | GSE41078 | GEO
Project description:Psoriasis is a common chronic inflammatory and hyperproliferative immune-mediated skin disorder. Narrow-band UVB (NB-UVB) phototherapy is a convenient first-line treatment of psoriasis, though the mechanisms underlying its efficacy have not been completely elucidated. In order to improve our understanding of NB-UVB phototherapy, gene expression profiling was used to characterize gene expression in lesional epidermis from psoriasis patients undergoing NB-UVB phototherapy. Increased expression of melanogenesis pathway genes was observed to be the earliest response. At the end of treatment, genes involved in diverse biological processes were affected, such as pigmentation, cell adhesion, ectodermal development and metabolism. The relationship between gene expression and treatment outcome was further studied using Partial Least Squares Discriminant Analysis (PLS-DA). Gene ontology analysis showed that genes responding to phototherapy and highly correlated to treatment outcome were involved in oxidation reduction, growth and mitochondria organization. In particular SPATA18, a key regulator of mitochondria quality, was found to be significantly downregulated in psoriasis, and its upregulation following phototherapy was required for optimal clinical improvement. Our data suggest that oxidation reduction is a critical event for the resolution of psoriatic plaques.
2013-12-23 | GSE53431 | GEO
Project description:We sought to define the cutaneous response at 24 hours following erythemogenic doses of narrow-band UVB (NB-UVB, 312 nm peak) exposure and determine the differences between irradiated and non-irradiated skin. Comparison of Transcriptome between NB-UVB irradiated (2MED) and non-irradiated skin (NON IRRAD).
2012-10-30 | E-GEOD-41078 | biostudies-arrayexpress
Project description:Psoriasis is a common chronic inflammatory and hyperproliferative immune-mediated skin disorder. Narrow-band UVB (NB-UVB) phototherapy is a convenient first-line treatment of psoriasis, though the mechanisms underlying its efficacy have not been completely elucidated. In order to improve our understanding of NB-UVB phototherapy, gene expression profiling was used to characterize gene expression in lesional epidermis from psoriasis patients undergoing NB-UVB phototherapy. Increased expression of melanogenesis pathway genes was observed to be the earliest response. At the end of treatment, genes involved in diverse biological processes were affected, such as pigmentation, cell adhesion, ectodermal development and metabolism. The relationship between gene expression and treatment outcome was further studied using Partial Least Squares Discriminant Analysis (PLS-DA). Gene ontology analysis showed that genes responding to phototherapy and highly correlated to treatment outcome were involved in oxidation reduction, growth and mitochondria organization. In particular SPATA18, a key regulator of mitochondria quality, was found to be significantly downregulated in psoriasis, and its upregulation following phototherapy was required for optimal clinical improvement. Our data suggest that oxidation reduction is a critical event for the resolution of psoriatic plaques. Twelve patients diagnosed with plaque type psoriasis were recruited to the study. NB-UVB irradiation was administered to the whole body two to three times a week. Treatment comprising approximately 24 sessions was given during two to three months. A total of six 4 mm diameter punch biopsies were taken from lesions on each psoriasis patient: two prior to UV treatment (pre-UV), two at the middle stage of UV treatment (after about one month of treatment, mid-UV) and two before the last treatment session (post-UV). Twelve healthy age-, sex- and skin type-matched volunteers were also recruited and two punch biopsies were taken from the buttocks. RNA was extracted from Laser capture microdissected epidermis.
2013-12-23 | E-GEOD-53431 | biostudies-arrayexpress
Project description:To obtain a comprehensive DNA methylation signature specific for the epidermal component of psoriasis and to analyze methylation changes during therapy, we performed genome-wide DNA methylation profiling of epidermal cells from 12 patients undergoing narrow-band UVB phototherapy and 12 corresponding healthy controls. A distinct DNA methylation pattern was seen in psoriasis compared to controls. An overall hypomethylation was found in psoriasis and 3665 methylation variable positions were identified. The DNA methylation pattern was reversed at the end of phototherapy in patients with clinical response.
2015-04-02 | GSE63315 | GEO
Project description:To obtain a comprehensive DNA methylation signature specific for the epidermal component of psoriasis and to analyze methylation changes during therapy, we performed genome-wide DNA methylation profiling of epidermal cells from 12 patients undergoing narrow-band UVB phototherapy and 12 corresponding healthy controls. A distinct DNA methylation pattern was seen in psoriasis compared to controls. An overall hypomethylation was found in psoriasis and 3665 methylation variable positions were identified. The DNA methylation pattern was reversed at the end of phototherapy in patients with clinical response. Bisulphite converted DNA from the 47 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip.
2015-04-02 | E-GEOD-63315 | biostudies-arrayexpress
Project description:Background: Atopic dermatitis (AD) is a common inflammatory skin disease exhibiting a predominantly Th2/“T22” immune activation and a defective epidermal barrier. Narrow-band UVB (NB-UVB) is considered an efficient treatment for moderate to severe AD. In psoriasis, NB-UVB has been found to suppress the Th1/Th17 immune polarization with subsequent reversal of epidermal hyperplasia. The immunomodulatory effects of this treatment are largely unknown in AD. Our study evaluates the effects of NB-UVB on immune and barrier abnormalities in AD, aiming to establish reversibility of disease and biomarkers of therapeutic response. Methods: 12 moderate-to-severe chronic AD patients received NB-UVB phototherapy 3 times weekly for up to 12 weeks. Lesional and non-lesional skin biopsies were obtained before and after treatment and evaluated by gene-expression and immunohistochemistry studies. Results: All patients had at least a 50% reduction in SCORing of AD (SCORAD) index with NB-UVB phototherapy. The Th2, T22, and Th1 immune pathways were suppressed and measures of epidermal hyperplasia and differentiation also normalized after phototherapy. The reversal of disease activity was associated with elimination of inflammatory leukocytes, Th2/“T22”-associated cytokines and chemokines, and normalized expression of barrier proteins. Conclusions: Our study shows reversal of both the epidermal defects and underlying immune activation in AD. By determining the correlation of variables with therapeutic response, we have defined a set of biomarkers of disease response that associate resolved Th2 and T22 inflammation with reversal of barrier pathology. This data supports the “inside-out” hypothesis of AD, suggesting that it is a disease primarily driven by an immune stimulus.
2011-07-01 | GSE27887 | GEO
Project description:Background: Atopic dermatitis (AD) is a common inflammatory skin disease exhibiting a predominantly Th2/"T22" immune activation and a defective epidermal barrier. Narrow-band UVB (NB-UVB) is considered an efficient treatment for moderate to severe AD. In psoriasis, NB-UVB has been found to suppress the Th1/Th17 immune polarization with subsequent reversal of epidermal hyperplasia. The immunomodulatory effects of this treatment are largely unknown in AD. Our study evaluates the effects of NB-UVB on immune and barrier abnormalities in AD, aiming to establish reversibility of disease and biomarkers of therapeutic response. Methods: 12 moderate-to-severe chronic AD patients received NB-UVB phototherapy 3 times weekly for up to 12 weeks. Lesional and non-lesional skin biopsies were obtained before and after treatment and evaluated by gene-expression and immunohistochemistry studies. Results: All patients had at least a 50% reduction in SCORing of AD (SCORAD) index with NB-UVB phototherapy. The Th2, T22, and Th1 immune pathways were suppressed and measures of epidermal hyperplasia and differentiation also normalized after phototherapy. The reversal of disease activity was associated with elimination of inflammatory leukocytes, Th2/"T22"-associated cytokines and chemokines, and normalized expression of barrier proteins. Conclusions: Our study shows reversal of both the epidermal defects and underlying immune activation in AD. By determining the correlation of variables with therapeutic response, we have defined a set of biomarkers of disease response that associate resolved Th2 and T22 inflammation with reversal of barrier pathology. This data supports the "inside-out" hypothesis of AD, suggesting that it is a disease primarily driven by an immune stimulus. genomic profiling of treatment effect of NB-UVB in AD in both lesional and non-lesional AD skin from 10 patients. Treatment effect, disease state analysis
2011-07-01 | E-GEOD-27887 | biostudies-arrayexpress
Project description:In repigmentation of human vitiligo, the melanocyte (MC) precursors in the hair follicle (HF) bulge proliferate, migrate and differentiate to repopulate the depigmented epidermis. Here we present a comprehensive characterization of pathways and signals in the bulge that control the repigmentation process. Using biopsies from vitiligo patients we have selectively harvested, by laser capture microdissection, MC and keratinocyte precursors from the HF bulge of untreated vitiligo skin and vitiligo skin treated with Narrow Band UVB (NBUVB). The captured material was subjected to whole transcriptome RNA sequencing. With this strategy, we found that repigmentation in the bulge MCs precursors is driven by KCTD10, a signal with unknown roles in the skin, and by CTNNB1 (encoding β-catenin) and RHO-GTPase (RHO), two signaling pathways previously shown to be involved in pigmentation biology.
2020-11-01 | GSE150954 | GEO