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HCV poly U/UC sequences induced abnormal inflammation leads to metabolic disorders in Vulvar Lichen Sclerosis

ABSTRACT: HCV poly U/UC sequences induced abnormal inflammation leads to metabolic disorders in Vulvar Lichen Sclerosis

PROVIDER: PRJNA701431 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13687700_1.fastq.gz	Fastqsanger.gz
	SRR13687700_2.fastq.gz	Fastqsanger.gz
	SRR13687701_1.fastq.gz	Fastqsanger.gz
	SRR13687701_2.fastq.gz	Fastqsanger.gz
	SRR13687702_1.fastq.gz	Fastqsanger.gz

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HCV poly U/UC sequences induced abnormal inflammation leads to metabolic disorders in Vulvar Lichen Sclerosis

Project description:While VLS is a serious skin disease affecting women in an annoying, embarrassing, and prolonged way worldwide, its pathogenesis and molecular characteristics are still unexploreed. Previous studies have suggested the correlation between inflammation or microRNA and VLS, but the lack of comprehensive understanding on its mechanism prevents the development of precision medicine for it. For a long time, VLS has been speculated as an autoimmune disease (Tran, Tan et al., 2019). This hypothesis was derived from several clinical observations: (1) VLS is frequently observed in women with an autoimmune diseases called Turner Syndrome (Chakhtoura, Vigoureux et al., 2014) ; (2) Many VLS patients also develop various autoimmune diseases (Kreuter, Kryvosheyeva et al., 2013, Song, Xiaoli et al., 2018) ; (3) VLS patients may also have higher frequency of certain HLA antigens, though few immunological consequence has been studied (Sideri, Rognoni et al., 1988). Microarray assay found upregulation of Th1, microRNA-155 and relative transcripts using VLS and healthy donors biopsies (Ren, Zhao et al., 2018, Terlou, Santegoets et al., 2012). However, the person-to-person genotype variation can hardly eliminate without using normal tissues from the same patient; and the PCR-based measurement of transcriptome of microarray limited the data interpretation and assumption validation. In this article, we performed multi-omics analyses on VLS paired-samples from the same patients as well as the normal ones from healthy donors. RNA-seq analysis revealed VLS patients are suffering from abnormally high inflammation with impressive anti-virus features. In-depth analysis of their transcriptome identified a remarkable enrichment of HCV poly U/UC sequence in VLS transcriptome, which might contribute to the onset of VLS. Multi-omics results indicated various inflammation-induced metabolic disorders in VLS samples, which might serve as therapeutic targets for precision medicine.

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HCV poly U/UC sequence-induced inflammation leads to metabolic disorders in vulvar lichen sclerosis.

Project description:Vulvar lichen sclerosis (VLS) is a dermatologic disorder that affects women worldwide. Women with VLS have white, atrophic papules on the vulva. They suffer from life-long intense pruritus. Corticosteroids are the first-line of treatments and the most effective medicines for VLS. Although VLS has been speculated as an autoimmune disease for a long time, its pathogenesis and the molecular mechanism is largely unknown. We performed a comprehensive multi-omics analysis of paired samples from VLS patients as well as healthy donors. From the RNA-seq analysis, we found that VLS is correlated to abnormal antivirus response because of the presence of Hepatitis C Virus poly U/UC sequences. Lipidomic and metabolomic analysis revealed that inflammation-induced metabolic disorders of fatty acids and glutathione were likely the reasons for pruritus, atrophy, and pigment loss in the vulva. Thus, the present study provides an initial interpretation of the pathogenesis and molecular mechanism of VLS and suggests that metabolic disorders that affect the vulva may serve as therapeutic targets for VLS.

| S-EPMC8321666 | biostudies-literature

MicroRNAs expression in vulvar lichen sclerosus keratinocytes and fibroblasts: further evidence and possible pathogenetic implications from an observational study

Project description:It seems established that genetic and epigenetic determinants drive the multifactorial pathogenic processes in vulvar lichen sclerosus (VLS). Aberrant expression of microRNAs (miRNAs) has been observed in a few studies suggesting potential involvement. We aimed to assess the expression of miRNAs both in VLS and in healthy keratinocytes and fibroblasts cultured separately. The differential analysis led to the identification of 171 and 111 microRNAs with an expression difference of at least 1.5-fold between VLS and healthy samples, in keratinocytes and fibroblasts, respectively. More than 80% of the 111 microRNAs identified as differentially expressed in fibroblasts were also found to be differentially expressed in keratinocytes. A number of dysregulated miRNAs are involved in inflammation and fibrotic processes, namely miR-10a-5p and 3p, miR-143-3p and 5p, miR-181a-5p and 3p, miR-181b-5p and 3p, miR-21-3p, miR-146b-5p and miR-29c. Our results showed a clear separation of VLS keratinocytes and fibroblasts from healthy cells in terms of miRNA expression. It is noteworthy that the most dysregulated miRNAs are implicated in inflammatory and fibrotic pathways. It is conceivable that miRNA expression is functional in regulating pathogenetic mechanisms of LS.

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Project description:Vulvar lichen sclerosus (LS) is a chronic, inflammatory dermatosis that may lead to scarring of the vulva and sexual dysfunction. LS affects women of all ages and often goes unrecognized and underreported. Uncertainty continues to exist around its pathogenesis, histologic diagnosis, and treatment. However, there have been great advances in our understanding of autoimmunogenic targets in disease formation and progression. In addition, there has been recent investigation of potential non-steroid-based treatments, including platelet-rich plasma therapy and energy-based modalities such as the fractional CO2 laser, photodynamic therapy, and high intensity focused ultrasound. Refinement of surgical techniques for restoring vulvar anatomy and treating clitoral phimosis, introital stenosis, and vulvar granuloma fissuratum is leading to improved patient outcomes. This review summarizes current perspectives on the pathogenesis, symptomatology, diagnosis, and treatment for vulvar lichen sclerosus.

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Gene expression profiling of oral and genital lichen planus epithelium and normal oral and genital epithelium

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