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BioMed Research International
Volume 2017 (2017), Article ID 7479523, 15 pages
Research Article

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

1Department of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China
2Yan’an Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China

Correspondence should be addressed to Li He; moc.361@3662ileh

Received 2 May 2017; Revised 11 August 2017; Accepted 28 September 2017; Published 14 November 2017

Academic Editor: Konstantinos Papatheodorou

Copyright © 2017 Dongyun Lei et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.