Long non‐coding RNAs in cutaneous biology and proliferative skin diseases: Advances and perspectives

Tang, Lin; Liang, Yongxin; Xie, Hesong; Yang, Xiaozhi; Zheng, Guangjuan

doi:10.1111/cpr.12698

Cited by 41 publications

(29 citation statements)

References 117 publications

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“…Two major classes of non-coding RNA play a role in the pathogenesis of psoriasis: long non-coding RNA (lncRNA) and microRNA (miRNA) [32][33][34][35][36].…”

Section: Non-coding Rnamentioning

confidence: 99%

The Role of Epigenetic Factors in Psoriasis

Dopytalska

Ciechanowicz

Wiszniewski

et al. 2021

IJMS

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Psoriasis is a chronic, systemic, immune-mediated disease with an incidence of approximately 2%. The pathogenesis of the disease is complex and not yet fully understood. Genetic factors play a significant role in the pathogenesis of the disease. In predisposed individuals, multiple trigger factors may contribute to disease onset and exacerbations of symptoms. Environmental factors (stress, infections, certain medications, nicotinism, alcohol, obesity) play a significant role in the pathogenesis of psoriasis. In addition, epigenetic mechanisms are considered result in modulation of individual gene expression and an increased likelihood of the disease. Studies highlight the significant role of epigenetic factors in the etiology and pathogenesis of psoriasis. Epigenetic mechanisms in psoriasis include DNA methylation, histone modifications and non-coding RNAs. Epigenetic mechanisms induce gene expression changes under the influence of chemical modifications of DNA and histones, which alter chromatin structure and activate transcription factors of selected genes, thus leading to translation of new mRNA without affecting the DNA sequence. Epigenetic factors can regulate gene expression at the transcriptional (via histone modification, DNA methylation) and posttranscriptional levels (via microRNAs and long non-coding RNAs). This study aims to present and discuss the different epigenetic mechanisms in psoriasis based on a review of the available literature.

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“…Two major classes of non-coding RNA play a role in the pathogenesis of psoriasis: long non-coding RNA (lncRNA) and microRNA (miRNA) [32][33][34][35][36].…”

Section: Non-coding Rnamentioning

confidence: 99%

The Role of Epigenetic Factors in Psoriasis

Dopytalska

Ciechanowicz

Wiszniewski

et al. 2021

IJMS

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“…They also identified distinct tissue-specific expression patterns and epigenetic profiles for novel lncRNAs. Altogether, these results indicate that great deals of lncRNAs are involved in the immune pathogenesis of psoriasis [ 87 , 91 ].…”

Section: Long Non-coding Rna In Psoriasismentioning

confidence: 99%

“…lncRNA are involved in epigenetic silencing, splicing process regulation, translation control, regulating the apoptosis and cell cycle control. Moreover, the expression levels of various lncRNA are closely related to epidermal differentiation and immunoregulation [85][86][87][88][89][90][91][92][93]. There are many examples illustrating that ln-cRNAs are also involved in regulation of a variety of skin pathological conditions including skin cancer, wound healing and psoriasis [85][86][87][88].…”

Section: Long Non-coding Rna In Psoriasismentioning

confidence: 99%

Pathogenesis of psoriasis in the “omic” era. Part II. Genetic, genomic and epigenetic changes in psoriasis

Nedoszytko¹,

Szczerkowska‐Dobosz²,

Stawczyk-Macieja³

et al. 2020

pdia

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Psoriasis is a multifactorial disease in which genetic, environmental and epigenetic factors regulating gene expression play a key role. In the “genomic era”, genome-wide association studies together with target genotyping platforms performed in different ethnic populations have found more than 50 genetic susceptible markers associated with the risk of psoriasis which have been identified so far. Up till now, the strongest association with the risk of the disease has been proved for HLA-C*06 gene. The majority of other psoriasis risk SNPs are situated near the genes encoding molecules involved in adaptive and innate immunity, and skin barrier function. Many contemporary studies indicate that the epigenetic changes: histone modification, promoter methylations, long non-coding and micro-RNA hyperexpression are considered as factors contributing to psoriasis pathogenesis as they regulate abnormal keratinocyte differentiation and proliferation, aberrant keratinocytes – inflammatory cells communication, neoangiogenesis and chronic inflammation. The circulating miRNAs detected in the blood may become specific markers in the diagnosis, prognosis and response to the treatment of the disease. The inhibition of expression in selected miRNAs may be a new promising therapy option for patients with psoriasis.

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“…The transcript of maternally expressed gene 3 ( MEG3 ) is an lncRNA that does not encode for protein and has regulatory effect on cell function (Zhang , 2018 ; Tang et al 2020 ; Chanda 2018 ). Recent studies have shown that the abnormal expression of MEG3 in placental villi is closely associated with the preeclampsia and MEG3 can regulate the proliferative and invasive capacities of trophoblasts (Zhang 2015 ; Yu 2018 ).…”

Section: Introductionmentioning

confidence: 99%

The long noncoding RNA MEG3 regulates Ras-MAPK pathway through RASA1 in trophoblast and is associated with unexplained recurrent spontaneous abortion

Zhang

Liu

Gao

2021

Mol Med

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Background Maternally Expressed Gene 3 (MEG3) is expressed at low levels in placental villi during preeclampsia; however, its roles in unexplained recurrent spontaneous abortion (URSA) remain unclear. In this study, we aimed to explore the relationship between MEG3 and URSA. Methods The differentially expressed lncRNAs (MEG3) and its downstream genes (RASA1) were identified using bioinformatics analysis of Genomic Spatial Event (GSE) database. The expression levels of MEG3 in embryonic villis (with gestational ages of 49–63 days) and primary trophoblasts were determined using quantitative RT-PCR assay. A mouse model of Embryo implantation, Cell Counting Kit-8 (CCK-8), flow cytometry, and Transwell migration assays were performed to determine the implantation, proliferative, apoptotic, and invasive capacities of trophoblast. The level of phosphorylated core proteins in the RAS-MAPK pathway were analyzed using Western blot assay. The mechanisms of MEG3 in the regulation of RASA1 were studied by RNA pulldown, RNA immunoprecipitation (RIP), DNA pulldown, and chromatin immunoprecipitation (ChIP) assays. Results MEG3 had a low expression level in embryonic villis of 102 URSA patients compared with those of 102 normal pregnant women. MEG3 could promote proliferation and invasion, inhibit the apoptosis of primary trophoblast of URSA patients (PT-U cells), as well as promote embryo implantation of mouse. Besides, MEG3 also promoted the phosphorylation of rapidly accelerated fibrosarcoma (Raf), mitogen-activated protein kinase kinase (MEK), and extracellular-signal-regulated kinase (ERK) proteins. The results of RNA pull down and RIP assays showed that MEG3 bound with the enhancer of zeste homolog 2 (EZH2). The DNA pulldown assay revealed that MEG3 could bind to the promoter sequence of the RAS P21 Protein Activator 1 (RASA1) gene. Further, the ChIP assay showed that MEG3 promoted the binding of EZH2 to the promoter region of the RASA1 gene. Conclusions The inactivation of MEG3 in embryonic villi association with URSA; MEG3 inhibited the expression of RASA1 by mediating the histone methylation of the promoter of RASA1 gene by EZH2, thereby activating the RAS-MAPK pathway and enhancing the proliferative and invasive capacities of trophoblasts.

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Long non‐coding RNAs in cutaneous biology and proliferative skin diseases: Advances and perspectives

Cited by 41 publications

References 117 publications

The Role of Epigenetic Factors in Psoriasis

The Role of Epigenetic Factors in Psoriasis

Pathogenesis of psoriasis in the “omic” era. Part II. Genetic, genomic and epigenetic changes in psoriasis

The long noncoding RNA MEG3 regulates Ras-MAPK pathway through RASA1 in trophoblast and is associated with unexplained recurrent spontaneous abortion

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