MiR‐146a regulates PM1‐induced inflammation via NF‐κB signaling pathway in BEAS‐2B cells

• Published in: Environmental toxicology Vol. 33; no. 7; pp. 743 - 751
• Main Authors: Liu, Limin, Wan, Chong, Zhang, Wei, Guan, Longfei, Tian, Guoxiong, Zhang, Fang, Ding, Wenjun
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc 01.07.2018
• Subjects: Aerodynamics; Asthma; BEAS‐2B cells; Biocompatibility; Cancer; Cells; Chronic obstructive pulmonary disease; Exposure; Inflammation; Inflammatory response; IRAK protein; Lung cancer; Lungs; miRNA; miR‐146a; NF‐κB; Nuclear transport; Particulate emissions; Particulate matter; PM1; Signal transduction; Signaling; Suspended particulate matter; Toxicity; TRAF6 protein; Translocation
• ISSN: 1520-4081; 1522-7278
• DOI: 10.1002/tox.22561

Exposure to particulate matter (PM) leads to kinds of cardiopulmonary diseases, such as asthma, COPD, arrhythmias, lung cancer, etc., which are related to PM‐induced inflammation. We have found that PM2.5 (aerodynamics diameter <2.5 µm) exposure induces inflammatory response both in vivo and in vitro. Since the toxicity of PM is tightly associated with its size and components, PM1 (aerodynamics diameter <1.0 µm) is supposed to be more toxic than PM2.5. However, the mechanism of PM1‐induced inflammation is not clear. Recently, emerging evidences prove that microRNAs play a vital role in regulating inflammation. Therefore, we studied the regulation of miR‐146a in PM1‐induced inflammation in human lung bronchial epithelial BEAS‐2B cells. The results show that PM1 induces the increase of IL‐6 and IL‐8 in BEAS‐2B cells and up‐regulates the miR‐146a expression by activating NF‐κB signaling pathway. Overexpressed miR‐146a prevents the nuclear translocation of p65 through inhibiting the IRAK1/TRAF6 expression, and downregulates the expression of IL‐6 and IL‐8. Taken together, these results demonstrate that miR‐146a can negatively feedback regulate PM1‐induced inflammation via NF‐κB signaling pathway in BEAS‐2B cells.