Accumulating evidence reveals that exosome plays an important role in cell-to-cell communication in both physiological and pathological processes by transferring bioactive molecules. However, the role of exosomal secretion in the adaption of its source cells to the stimuli of environmental chemicals remains elusive. In this study, we revealed that the exposure of hydroquinone (HQ; the main bioactive metabolite of benzene) to human bronchial epithelial cells (16HBE) resulted in decreased ability of cell proliferation and migration, and simultaneously DNA damage and micronuclei formation. Interestingly, when exosomal secretion of HQ treated 16HBE cells was inhibited with the inhibitor GW4869, cellular proliferation and migration were further significantly reduced; concurrently, their DNA damage and micronuclei formation were both further significantly aggravated. Herein, we conclude that exosomal secretion of 16HBE cells may be an important self-protective function against the toxic effects induced by HQ.
Myocardial infarction (MI), a life-threatening cardiac event, results in extreme damage to the heart muscle. In this study, we were committed to exploring the role and related mechanisms of microRNA-181a-5p (miR-181a-5p) in MIin vitro. Firstly, we established the MIin vitro cell model by subjecting H9c2 cells to hypoxia. We found that miR-181a-5p was significantly increased in hypoxia-induced H9c2 cells. Then, TargetScan and dual luciferase reporter gene assay confirmed the binding sites between Sirtuin 1 (SIRT1) and miR-181a-5p. SIRT1 was significantly reduced in hypoxia-induced H9c2 cells. Next, we explored the effect of miR-181a-5p inhibitor on hypoxiainduced H9c2 cell injury. The findings indicated that miR-181a-5p inhibitor significantly reduced creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI) production enhanced by hypoxia treatment. Moreover, miR-181a-5p inhibitor increased mitochondrial viability in hypoxia-induced H9c2 cells. MTT assay showed that miR-181a-5p inhibitor enhanced hypoxia-induced H9c2 cell viability, and flow cytometry assay indicated that miR-181a-5p inhibitor reduced H9c2 cell apoptosis. ELISA assay indicated that compared with hypoxia treatment group, miR-181a-5p inhibitor decreased the secretion of inflammatory factor such as IL-6, TNF-α and IL-1β . Finally, Western blot assay showed that miR-181a-5p inhibitor decreased the expression of p-p65, indicating the inhibition on NF- κB signaling pathway activation. However, all these effects of miR-181a-5p inhibitor on hypoxia-induced H9c2 cells were reversed by SIRT1-siRNA. Taken together, miR-181a-5p inhibitor protected against hypoxia-induced H9c2 cell injury by targeting SIRT1.
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