Increased miR-424-5p expression in peripheral blood mononuclear cells from patients with pemphigus

نویسندگان

  • Menglei Wang
  • Liuping Liang
  • Li Li
  • Kai Han
  • Qian Li
  • Yusheng Peng
  • Xuebiao Peng
  • Kang Zeng
چکیده

Pemphigus is an autoimmune disease that causes blisters and erosions in the skin and mucous membranes. The development of pemphigus is associated with the imbalance of T‑cell and humoral responses. MicroRNAs (miRNAs) can regulate many cell functions. However, whether miRNA expression is altered in peripheral blood mononuclear cells (PBMCs) during the pathogenesis of pemphigus has not been clarified. The aim of the present study was to examine the miRNA expression profiles of PBMCs from patients with pemphigus. The expression profiles of miRNAs in PBMCs from patients with active pemphigus (n=3) and healthy subjects (n=3) were analyzed by microarray. The relative levels of miR-424-5p expression in PBMCs from 9 patients and controls were validated by RT-qPCR. The functional and biological processes of the differentially expressed miRNAs were analyzed by bioinformatics. There were 124 differentially expressed miRNAs in PBMCs from the patients with pemphigus, compared with healthy controls, including 71 that were upregulated (P<0.05, fold change >2), and 53 that were downregulated (P<0.05, fold change <0.5). miR-424-5p was highly expressed in patients with pemphigus. Bioinformatics analysis indicated that the genes targeted by miR-424-5p were involved in intracellular signaling cascades, phosphate metabolism and regulation of kinase activity. The predicted target genes were associated with the T-cell receptor and mitogen-activated protein kinase signaling pathways as well as others. In conclusion, the results have demonstrated the miRNA expression profile, and verified that miR-424-5p was upregulated in PBMCs from patients with pemphigus. The biological function and potential pathways of miR-424-5p in pemphigus were predicted. Thus, miR-424-5p may contribute to the pathogenesis of pemphigus.

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عنوان ژورنال:

دوره 15  شماره 

صفحات  -

تاریخ انتشار 2017