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慢性光化性皮炎中 mRNA 和长链非编码 RNA 谱的全基因组分析。

Genome-Wide Analysis of mRNA and Long Noncoding RNA Profiles in Chronic Actinic Dermatitis.

机构信息

Department of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.

Yan'an Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.

出版信息

Biomed Res Int. 2017;2017:7479523. doi: 10.1155/2017/7479523. Epub 2017 Nov 14.

DOI:10.1155/2017/7479523
PMID:29359156
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5735319/
Abstract

Chronic actinic dermatitis (CAD), a photosensitive dermatosis, is characterized by inflammatory lesions, especially on sun-exposed skin. However, its pathogenesis remains unclear. In this study, second-generation RNA sequencing and comprehensive bioinformatics analyses of mRNAs and long noncoding RNAs (lncRNAs) were performed to determine the transcriptome profiles of patients with CAD. A total 6889 annotated lncRNAs, 341 novel lncRNAs, and 65091 mRNAs were identified. Interestingly, patients with CAD and healthy controls showed distinct transcriptome profiles. Indeed, 198 annotated (81.48%) and 45 novel (18.52%) lncRNAs were differentially expressed between the two groups. GO, KEGG, and RGSEA analyses of lncRNAs showed that inflammatory and immune response related pathways played crucial roles in the pathogenetic mechanism of CAD. In addition, we unveiled key differentially expressed lncRNAs, including lncRNA RP11-356I2.4 which plays a role probably by regulating TNFAIP3 and inflammation. qRT-PCR data validated the differentially expressed genes. The newly identified lncRNAs may have potential roles in the development of CAD; these findings lay a solid foundation for subsequent functional exploration of lncRNAs and mRNAs as therapeutic targets for CAD.

摘要

慢性光化性皮炎（CAD）是一种光敏性皮炎，其特征为炎症性病变，尤其出现在暴露于阳光下的皮肤。然而，其发病机制尚不清楚。在这项研究中，我们对 CAD 患者的 mRNA 和长链非编码 RNA（lncRNA）进行了第二代 RNA 测序和综合生物信息学分析，以确定其转录组图谱。共鉴定出 6889 个注释 lncRNA、341 个新 lncRNA 和 65091 个 mRNA。有趣的是，CAD 患者和健康对照者表现出明显不同的转录组图谱。实际上，两组之间有 198 个注释（81.48%）和 45 个新的（18.52%）lncRNA 存在差异表达。lncRNA 的 GO、KEGG 和 RGSEA 分析表明，炎症和免疫反应相关途径在 CAD 的发病机制中起着关键作用。此外，我们揭示了关键的差异表达 lncRNA，包括 lncRNA RP11-356I2.4，其可能通过调节 TNFAIP3 和炎症发挥作用。qRT-PCR 数据验证了差异表达基因。新鉴定的 lncRNA 可能在 CAD 的发生发展中具有潜在作用；这些发现为随后对 lncRNA 和 mRNA 作为 CAD 治疗靶点的功能探索奠定了坚实的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760a/5735319/b523f5936cc0/BMRI2017-7479523.009.jpg
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