Abstract
BackgroundPsoriasis is a complex, chronic inflammatory skin disease with substantial negative effects on patient quality of life. Long non-coding RNAs (lncRNAs) are able to be involved in multitudes of cellular processes in diverse human diseases. This study aimed to investigate the potential involvement of lncRNA MIR31HG in HaCaT keratinocytes proliferation.ResultsThe study showed that MIR31HG was significantly elevated in the lesional psoriatic skin compared with normal individuals’ skin. Knockdown of MIR31HG inhibited HaCaT keratinocytes proliferation. Flow cytometry analysis showed that siRNA-mediated MIR31HG depletion induced cell cycle arrest in the G2/M phase. In addition, MIR31HG expression was found to be dependent on NF-κB activation.ConclusionsNF-κB activation mediated MIR31HG upregulation plays an important role in the regulation of HaCaT keratinocytes proliferation. It could be a potential diagnostic biomarker and therapeutic target for psoriasis.
Highlights
Psoriasis is a complex, chronic inflammatory skin disease with substantial negative effects on patient quality of life
Knockdown of miR-31 host gene (MIR31HG) inhibits HaCaT keratinocytes proliferation In order to determine the possible effects of aberrant MIR31HG expression on keratinocyte proliferation, we applied small interfering RNA (siRNA) targeting MIR31HG to suppress its expression in HaCaT keratinocytes. quantitative real-time PCR (qRT-PCR) assay showed that MIR31HG expression was significantly suppressed by specific siRNA (Fig. 2a)
Keratin 6 (KRT6) and keratin 16 (KRT16) are considered to be the hallmarks of psoriatic keratinocytes hyperproliferation [15,16,17]. qRT-PCR assay showed that MIR31HG knockdown resulted in significant reduction of the expression of KRT6 and KRT16 (Fig. 2d)
Summary
Chronic inflammatory skin disease with substantial negative effects on patient quality of life. Long non-coding RNAs (lncRNAs) are able to be involved in multitudes of cellular processes in diverse human diseases. Chronic inflammatory skin disease affecting 2–3% of the population worldwide [1]. Psoriasis lesions are characterized by epidermal hyperproliferation and aberrant differentiation of keratinocytes and infiltration of inflammatory cells into the dermis and epidermis, which manifests clinically in the thickening and scaling of skin lesions [3]. Long non-coding RNAs (lncRNAs) are defined as transcripts longer than 200 nucleotides, with no protein coding capacity [4]. Multiple lines of evidence link dysregulations of lncRNAs to diverse human diseases [6].
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