Increased expression of LOC100506314 in T cells from patients with vitiligo and contributed to the pathogenesis of vitiligo
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ABSTRACT:
PROVIDER: PRJNA847448 | ENA |
REPOSITORIES: ENA
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Project description:The aim of this study was to investigate the differential expression of long non-coding RNAs (lncRNAs) in T cells from patients with vitiligo and their roles in the pathogenesis of vitiligo. The expression profiles of the RNA transcripts in T cells from three patients with vitiligo and three controls were conducted using microarray analysis. These aberrantly-expressed genes were further validated using T cells from 41 patients with vitiligo and 28 controls. The biologic function of the specific lncRNAs was investigated using transfection, RNA pull-down assay plus proteomic approach and Western blotting. As the results, the expression levels of 134 genes, were significantly increased, whereas the expression levels 142 genes were significantly decreased in T cells from patients with vitiligo compared with the controls. After selection and validation, the expression levels of 11 genes increased and two genes decreased in T cells from patients with vitiligo. We confirmed that LOC100506314 could interact with the signal transducer and activator of transcription 3 (STAT3) and macrophage migration inhibitory factor (MIF). The transfection of LOC100506314 could suppress STAT3, AKT, and ERK phosphorylation and nuclear protein levels of p65. Finally, overexpressed LOC100506314 decreased the T cell expression of IL-6 and IL-17. In conclusion, among the lncRNAs, we found that the expression levels of LOC100506314 were increased in T cells from patients with vitiligo. LOC100506314 could bind to STAT3 and MIF and suppress the expression of IL-6 and IL-17 through the inhibition of the STAT3, AKT, ERK, and NF-κB pathway. Increased the expression of LOC100506314 in T cells could be a potential therapeutic strategy for vitiligo.
2023-09-27 | GSE205751 | GEO
Project description:Vitiligo is an acquired depigmentation of the skin inducing a marked alteration of the quality of life of affected individuals. Halting the disease progression and repigmenting the lesional skin represent the two faces of the therapeutic challenge in vitiligo. So far, none of them has been successfully addressed. Oxidative stress and immune system in genetically predisposed individuals participate to the complex pathophysiology of vitiligo. We performed a transcriptome and proteomic analysis on lesional, perilesional and non-depigmented skin of vitiligo patients compared to matched skin controls of healthy subjects. Our results show that the WNT pathway, implicated in melanocytes differentiation, was found to be altered in vitiligo skin. We demonstrated that the oxidative stress decreases WNT expression/activation in keratinocytes and in melanocytes. We developed an ex vivo skin model that remains functional up to 15 days. We then confirmed the decreased activation of the WNT pathway in human skin subjected to oxidative stress. Finally, using pharmacological agents that activate the WNT pathway, we treated the ex vivo depigmented skins from vitiligo patients and successfully induced the differentiation of resident stem cells into pre-melanocytes supporting further exploration of WNT activators to repigment vitiligo lesions. Total of 40 chips. 10 patients (3 biospies per patient: 1 lesional , 1 perilesional and 1 non lesional) ; 10 healthy volunteers (1biopsy in matched anatomical areas)
2015-10-01 | E-GEOD-65127 | biostudies-arrayexpress
Project description:lesional and non-lesional skin from vitiligo patients
2016-11-01 | GSE75819 | GEO
Project description:We identified the differentially expressed circular RNAs in vitiligo patients before and after treatment of methylprednisolone. We have completed the Arraystar Human circRNA Array V2 analysis of the 8 peripheral blood specimens. Whole blood samples (3 mL each) were collected by venipuncture into heparinized vacutainers from a total of four patients diagnosed with nonsegmental vitiligo before and after systemic glucocorticoid therapy (oral methylprednisolone tablets, 12mg daily for eight weeks).
2022-02-25 | GSE197415 | GEO
Project description:Vitiligo Blood Transcriptomics Provides New Insights into Disease Mechanisms and Identifies Potential Novel Therapeutic Targets Abstract Background: Significant gaps remain regarding the pathomechanisms underlying the autoimmune response in vitiligo (VL), where the loss of self-tolerance leads to the targeted killing of melanocytes. Specifically, there is incomplete information regarding alterations in the systemic environment that are relevant to the disease state. Methods: We undertook a genome-wide profiling approach to examine gene expression in the peripheral blood of VL patients and healthy controls in the context of our previously published VL-skin gene expression profile. We used several in silico bioinformatics-based analyses to provide new insights into disease mechanisms and suggest novel targets for future therapy. Results: Unsupervised clustering methods of the VL-blood dataset demonstrate a “disease-state”-specific set of co-expressed genes. Ontology enrichment analysis of 99 differentially expressed genes (DEGs) uncovers a down-regulated immune/inflammatory response, B-Cell antigen receptor (BCR) pathways, apoptosis and catabolic processes in VL-blood. There is evidence for both type I and II interferon (IFN) playing a role in VL pathogenesis. We used interactome analysis to identify several key blood associated transcriptional factors (TFs) from within (STAT1, STAT6 and NF-kB), as well as “hidden” (CREB1, MYC, IRF4, IRF1, and TP53) from the dataset that potentially affect disease pathogenesis. The TFs overlap with our reported lesional-skin transcriptional circuitry, underscoring their potential importance to the disease. We also identify a shared VL-blood and -skin transcriptional “hot spot” that maps to chromosome 6, and includes three VL-blood dysregulated genes (PSMB8, PSMB9 and TAP1) described as potential VL-associated genetic susceptibility loci. Finally, we provide bioinformatics-based support for prioritizing dysregulated genes in VL-blood or skin as potential therapeutic targets. Conclusions: We examined the VL-blood transcriptome in context with our (previously published) VL-skin transcriptional profile to address a major gap in knowledge regarding the systemic changes underlying skin-specific manifestation of vitiligo. Several transcriptional “hot spots” observed in both environments offer prioritized targets for identifying disease risk genes. Finally, within the transcriptional framework of VL, we identify five novel molecules (STAT1, PRKCD, PTPN6, MYC and FGFR2) that lend themselves to being targeted by drugs for future potential VL-therapy. We used microarrays to detail the global programme of gene expression underlying the disease state in vitiligo and established differentially expressed genes by comparing gene expression values from diseased patients to healthy controls.
2017-01-31 | GSE90880 | GEO
Project description:Vitiligo is an acquired depigmentation of the skin inducing a marked alteration of the quality of life of affected individuals. Halting the disease progression and repigmenting the lesional skin represent the two faces of the therapeutic challenge in vitiligo. So far, none of them has been successfully addressed. Oxidative stress and immune system in genetically predisposed individuaLesionalparticipate to the complex pathophysiology of vitiligo. We performed a transcriptome and proteomic analysis on lesional, perilesional and non-depigmented skin of vitiligo patients compared to matched skin controLesionalof healthy subjects. Our results show that the WNT pathway, implicated in melanocytes differentiation, was found to be altered in vitiligo skin. We demonstrated that the oxidative stress decreases WNT expression/activation in keratinocytes and in melanocytes. We developed an ex vivo skin model that remains functional up to 15 days. We then confirmed the decreased activation of the WNT pathway in human skin subjected to oxidative stress. Finally, using pharmacological agents that activate the WNT pathway, we treated the ex vivo depigmented skins from vitiligo patients and successfully induced the differentiation of resident stem celLesionalinto pre-melanocytes supporting further exploration of WNT activators to repigment vitiligo lesions.
2015-10-01 | GSE65127 | GEO
Project description:Vitiligo skin samples with an active inflammatory infiltrate were selected for gene expression profiling in order to identify inflammatory pathways that drive depigmentation in vitiligo. Total RNA was isolated from 10 deidentified human samples from formalin fixed, paraffin-embedded skin, 5 from vitiligo patients and 5 from controls. Control skin was age- and site-matched excision tips without pathology.
2013-12-12 | E-GEOD-53146 | biostudies-arrayexpress
Project description:Investigate the gene expression change in the blood of segmental vitiligo, generalized vitiligo and healthy individual.
2016-04-08 | GSE80009 | GEO
Project description:We performed scRNA-seq analyses on patient matched lesional and nonlesional skin from viitiligo patients using the 10x genomics platform to examine different cell populations and keratinocyte states that may contribute to vitiligo disease persistence.
2022-05-20 | GSE203262 | GEO
Project description:Vitiligo is a common autoimmune depigmented dermatology due to the destruction of melanocytes. Much evidence suggests that vitiligo is associated with systemic immune activation. Previous studies have focused on immune cell infiltration in and around lesion areas, while few studies have investigated the cell types and function of circulating immune cells in peripheral blood. We collected peripheral blood from five patients with progressive non-segmental vitiligo (PV) and three healthy controls (HC).Single-cell RNA sequencing(scRNA-seq) is used to investigate the mechanisms of peripheral immune responses in vitiligo patients.
2023-11-07 | GSE231794 | GEO