Increased expression of microRNA-338-3p contributes to production of Dsg3 antibody in pemphigus vulgaris patients

  • Authors:
    • Qingxiu Liu
    • Feiyi Cui
    • Menglei Wang
    • Hao Xiong
    • Xiaoming Peng
    • Liuping Liang
    • Li Li
    • Jing Zhang
    • Xuebiao Peng
    • Kang Zeng
  • View Affiliations

  • Published online on: April 26, 2018     https://doi.org/10.3892/mmr.2018.8934
  • Pages: 550-556
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Expression of microRNA-338-3p (miR-338-3p) was aberrantly elevated in pemphigus vulgaris (PV), although its role in PV is still unknown. The present study investigated the functional role and possible molecular mechanisms of miR-338-3p in PV. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to detect miR-338-3p expression in peripheral blood mononuclear cells (PBMCs) from patients with PV. Correlation with disease severity and anti-desmoglein 3 antibody (anti-Dsg3) titers were analyzed in patients with PV. The effects of overexpression and knockdown of miR-338-3p expression in PBMCs and effects on Th1 and Th2 cytokines were also examined using ELISA. The luciferase reporter analysis, RT-qPCR and western blot analysis were applied to investigate potential and functional target genes. The data showed that miR-338-3p expression was significantly upregulated in PV and the upregulation of miR-338-3p associated with disease severity and a high anti-Dsg3 antibody titer. Expression of miR-338-3p/mimic in healthy PBMCs significantly downregulated Th1 cytokine (IFN-γ) and upregulated Th2 cytokines (IL-4 and IL-10), whereas knockdown of miR-338-3p expression in PBMCs from patients with PV induced the reverse effects. Overexpression of miR-338-3p suppressed cell viability. Luciferase reporter, RT-qPCR and western blot assays idnicated that TNFR1-associated death domain protein (TRADD) was the direct and functional target of miR-338-3p. Increased expression of miR-338-3p contributed to the production of Dsg3 antibody by inhibiting TRADD expression to induce an imbalance in Th1/Th2 cell functions. Taken together, this study suggests that miR-338-3p may be used as a potential therapeutic target for PV treatment.
View Figures
View References

Related Articles

Journal Cover

July-2018
Volume 18 Issue 1

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Liu Q, Cui F, Wang M, Xiong H, Peng X, Liang L, Li L, Zhang J, Peng X, Zeng K, Zeng K, et al: Increased expression of microRNA-338-3p contributes to production of Dsg3 antibody in pemphigus vulgaris patients. Mol Med Rep 18: 550-556, 2018
APA
Liu, Q., Cui, F., Wang, M., Xiong, H., Peng, X., Liang, L. ... Zeng, K. (2018). Increased expression of microRNA-338-3p contributes to production of Dsg3 antibody in pemphigus vulgaris patients. Molecular Medicine Reports, 18, 550-556. https://doi.org/10.3892/mmr.2018.8934
MLA
Liu, Q., Cui, F., Wang, M., Xiong, H., Peng, X., Liang, L., Li, L., Zhang, J., Peng, X., Zeng, K."Increased expression of microRNA-338-3p contributes to production of Dsg3 antibody in pemphigus vulgaris patients". Molecular Medicine Reports 18.1 (2018): 550-556.
Chicago
Liu, Q., Cui, F., Wang, M., Xiong, H., Peng, X., Liang, L., Li, L., Zhang, J., Peng, X., Zeng, K."Increased expression of microRNA-338-3p contributes to production of Dsg3 antibody in pemphigus vulgaris patients". Molecular Medicine Reports 18, no. 1 (2018): 550-556. https://doi.org/10.3892/mmr.2018.8934