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Unraveling the expression of microRNA‐27a* & NKG2D in peripheral blood mononuclear cells and natural killer cells of pediatric systemic lupus erythematosus patients
Author(s) -
Sourour Shady K.,
Aboelenein Heba R.,
Elemam Noha M.,
Abdelhamid Amira K.,
Salah Samia,
Abdelaziz Ahmed I.
Publication year - 2017
Publication title -
international journal of rheumatic diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 41
eISSN - 1756-185X
pISSN - 1756-1841
DOI - 10.1111/1756-185x.13099
Subject(s) - nkg2d , peripheral blood mononuclear cell , microrna , immunology , transfection , medicine , natural killer cell , pathogenesis , biology , cell culture , in vitro , gene , cytotoxicity , biochemistry , genetics
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 RNA s (mi RNA s), 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 RNA s that might potentially target an essential activating receptor, NKG 2D in peripheral blood mononuclear cells ( PBMC s) and NK cells of SLE patients. Methods In silico analysis revealed miR‐27a* to potentially target NKG 2D messenger RNA ( mRNA ), hence PBMC s 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 PBMC s and NK cells of SLE patients. In contrast, NKG 2D was found to be downregulated in PBMC s and NK cells of SLE patients. Forcing the expression of miR‐27a* in PBMC s and NK cells enhances the expression of NKG 2D in SLE patients. Furthermore, the ligand of NKG 2D, ULBP 2, was found to be downregulated in the PBMC s of SLE patients. Conclusion The altered expression of the triad, miR‐27a* as well as NKG 2D and ULBP 2, is thought to be characteristic for NK cells in SLE patients. Hence, the ability of miR‐27a* to alter the expression of NKG 2D may provide a new groundwork for understanding the role of mi RNA s in NK cells of SLE patients.