Background: Sulfur mustard as a chemical warfare agent causes short and long-term pulmonary complications in its victims. MicroRNAs are known to act as remarkable regulators of biological pathways, monitoring, and treatment of diseases including respiratory problems. In this study, we investigated the expression of miR-106a-5p and miR-106b-5p, two regulators of TGF-β signaling, as well as their target molecule, TGFβ1I1, in peripheral blood mononuclear cells from SM-exposed individuals.
Materials and Methods: A total of 70 veterans with SM-induced pulmonary complications were examined and compared to 35 gender and age-matched healthy controls. After clinical examination and pulmonary function tests, the severity of pulmonary complications was classified. Total RNA was extracted from PBMCs and the purity of extracted RNA samples was evaluated by a NanoDrop 2000. The miR-106a-5p, miR-106b-5p, and TGFβ1I1 expression levels were measured by real-time RT-PCR.
Results: The miR-106a-5p expression levels were significantly increased in both mild (P=0.015) and severe groups compared with the control group. The miR-106b-5p expression levels were considerably elevated in the severe group TGFβ1I1 expression levels were notably reduced in the severe group compared with the control group. Although, a slight decrease in TGFβ1I1 expression levels was observed in the mild group compared with the control.
Conclusion: Our results indicate that exposure to sulfur mustard affects the expression of miR-106a-5p, miR-106b-5p, and their target gene, TGFβ1I1, in peripheral blood mononuclear cells. Considering the role of TGFβ1I1 in the regulation of TGF-β signaling, the mentioned changes might point to a potential mechanism by which SM exposure causes chronic pulmonary complications. In a ROC analysis, miR-106a-5p and miR-106b-5p potentially turned out to be a suitable diagnostic biomarker in the mild and severe categories of patients. Although, miR-106a-5p could be considered a better biomarker than miR-106b-5p.