Research Paper Volume 12, Issue 2 pp 1141—1158

Figure 7. MiR-29b-3p inhibited the expression of C1QTNF6 in vivo. The acute PM-exposed mouse model was constructed and miR-29b-3p antagomirs (29b-antago) or negative control antagomirs (NC-antago) were delivered through the tail vein of mice 24 h prior to the first PM exposure. (A) Real-time PCR analysis of C1QTNF6 expression in mouse models treated with 29b-antago or NC-antago. (B) Western blot analysis of C1QTNF6 expression in mouse models treated with 29b-antago or NC-antago. The optical densities of protein bands were shown in (C). Values represent mean ± SEM; *, P<0.05, compared with the NC-antago + PM group; #, &, P<0.05, compared with the NC-antago group; n=3-5. (D) Immunohistological analysis of C1QTNF6 expression in lung tissue of mouse models treated with 29b-antago or NC-antago. (E) Schematic diagram of the critical role of miR-29b-3p in the PM-induced inflammatory responses. miR-29b-3p was upregulated by PM exposure and inhibited the activation of AMPK pathway via targeting C1QTNF6 to promote PM-induced inflammatory responses. PM, particulate matter.