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- Title
Unraveling the expression of microRNA-27a* & NKG2D in peripheral blood mononuclear cells and natural killer cells of pediatric systemic lupus erythematosus patients.
- Authors
Sourour, Shady K.; Aboelenein, Heba R.; Elemam, Noha M.; Abdelhamid, Amira K.; Salah, Samia; Abdelaziz, Ahmed I.
- Abstract
Background and aim The activity of natural killer ( NK) cells is known to be decreased in systemic lupus erythematosus ( SLE) patients. Nevertheless, the exact contribution of NK cells in the pathogenesis of SLE is still inconclusive. Micro RNAs (mi RNAs), are small noncoding RNA molecules that play a fundamental role in regulating NK cell function. The objective of this study was to investigate the expression of mi RNAs that might potentially target an essential activating receptor, NKG2D in peripheral blood mononuclear cells ( PBMCs) and NK cells of SLE patients. Methods In silico analysis revealed miR-27a* to potentially target NKG2D messenger RNA ( mRNA), hence PBMCs and NK cells were isolated from blood samples of SLE patients and healthy controls. Next, the cells were transfected using mimics and antagomirs, after which mi RNA/ mRNA were quantified using real time quantitative reverse transcription polymerase chain reaction. Results The results of this study showed that miR-27a* is overexpressed in the PBMCs and NK cells of SLE patients. In contrast, NKG2D was found to be downregulated in PBMCs and NK cells of SLE patients. Forcing the expression of miR-27a* in PBMCs and NK cells enhances the expression of NKG2D in SLE patients. Furthermore, the ligand of NKG2D, ULBP2, was found to be downregulated in the PBMCs of SLE patients. Conclusion The altered expression of the triad, miR-27a* as well as NKG2D and ULBP2, is thought to be characteristic for NK cells in SLE patients. Hence, the ability of miR-27a* to alter the expression of NKG2D may provide a new groundwork for understanding the role of mi RNAs in NK cells of SLE patients.
- Subjects
KILLER cells; GENE expression; MESSENGER RNA; SYSTEMIC lupus erythematosus; GENETIC overexpression
- Publication
International Journal of Rheumatic Diseases, 2017, Vol 20, Issue 9, p1237
- ISSN
1756-1841
- Publication type
Article
- DOI
10.1111/1756-185X.13099