Hautamaki RD, Kobayashi DK, Senior RM, Shapiro SD. Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs in the respiratory tract: potential implications in asthma and other lung diseases. Gueders MM, Foidart JM, Noel A, Cataldo DD. The microprocessor complex mediates the genesis of microRNAs. Gregory RI, Yan KP, Amuthan G, Chendrimada T, Doratotaj B, Cooch N, et al. Transgenic expression of matrix metalloproteinase-9 causes adult-onset emphysema in mice associated with the loss of alveolar elastin. 2006 61(3):259–66.įoronjy R, Nkyimbeng T, Wallace A, Thankachen J, Okada Y, Lemaitre V, et al. Matrix metalloproteinases in destructive pulmonary pathology. The role of miR-155 in cigarette smoke-induced pulmonary inflammation and COPD. 2017 18(1):4.ĭe Smet EG, Van Eeckhoutte HP, Avila Cobos F, Blomme E, Verhamme FM, Provoost S, et al. Bioinformatic analysis of microRNA and mRNA regulation in peripheral blood mononuclear cells of patients with chronic obstructive pulmonary disease. The m(6)A methyltransferase METT元 promotes bladder cancer progression via AFF4/NF-kappaB/MYC signaling network. Matrix metalloproteinases: a tail of a frog that became a prince. N6-methyladenosine marks primary microRNAs for processing. Update on the pathogenesis of chronic obstructive pulmonary disease. ![]() EV miR-93 may use as a novel risk biomarker for CS-induced emphysema. These results demonstrate that METT元-mediated formation of EV miR-93, facilitated by m6A, is implicated in the aberrant cross-talk of epithelium–macrophages, indicating that this process is involved in the smoking-related emphysema. In macrophages, miR-93 activated the JNK pathway by targeting dual-specificity phosphatase 2 (DUSP2), which elevated the levels of matrix metalloproteinase 9 (MMP9) and matrix metalloproteinase 12 (MMP12) and induced elastin degradation, leading to emphysema. Mature miR-93 was transferred from bronchial epithelial cells into macrophages by EVs. Here, we established that production of excess mature microRNA-93 (miR-93) in bronchial epithelial cells via enhanced m6A modification was mediated by overexpressed methyltransferase-like 3 (METT元) induced by CS. The formation of N6-methyladenosine (m6A) is a modification in miRNA processing, but its role in the development of emphysema remains unclear. Aberrant cross-talk between macrophages and bronchial epithelial cells is essential for the degradation of elastin that contributes to emphysema, in which extracellular vesicles (EVs) play a critical role. Cigarette smoke (CS), a complex chemical indoor air pollutant, induces degradation of elastin, resulting in emphysema.
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