Background
With little attention given to low‐frequency traffic noise and our understanding that cochlear function may be highly susceptible to low‐frequency noise, there is an urgent need to determine traffic noise‐induced hearing loss (NIHL), not only the hearing loss at low frequency but also the possible high‐frequency hearing loss.
Methods
The current study aims to investigate the potential for extensive hearing loss induced by exposure to 0.063 kHz octave band noise (OBN), which is an important component of low‐frequency traffic noise. The threshold of auditory brainstem response (ABR) was used to evaluate hearing function before and after noise exposure. Chinchillas were randomly assigned into seven different groups. Group 63‐3 h/6 h, Group 2 k‐3 h/6 h, and group 4 k‐3 h/6 h were exposed for either 3 or 6 h to 0.063, 2, and 4 kHz OBN at 90 dB SPL, respectively. The control group was not exposed to noise.
Results
Significant ABR threshold‐shifts (TS) were observed at 0.88, 2, 4, and 5.7 kHz in Group 63‐6 h, and at 2.8 and 4 kHz in Group 2 k‐6 h, and at 5.7 kHz in Group 4 k‐6 h. ABR‐TS were consistent with outer hair cell (OHC) losses, exposure to 0.063 kHz OBN at 90 dB SPL for 6 h induced large‐scale losses of OHC both in low‐ and high‐frequency region.
Conclusions
Exposure to 0.063 kHz low‐frequency OBN at 90 dB SPL for 6 h leads to significant hearing loss over an extensive range from low to high frequencies.
MicroRNAs (miR) are a class of non-coding endogenous RNA molecules that suppress the translation of protein-coding genes by destabilizing target mRNAs. The MiR-574-5p has been reported to be involved in the several types of cancer. However, the expression of miR-574-5p and its mechanism in nasopharyngeal carcinoma (NPC) remain unclear. We found that the expression level of miR-574-5p was significantly increased in the NPC cell lines. We further demonstrated that Forkhead box N3 (FOXN3) was a target gene of miR-574-5p. FOXN3 overexpression and inhibition reversed the promoting or suppressing effect, respectively, of NPC cell proliferation, migration and invasion caused by miR-574-5p. Furthermore, miR-574-5p enhanced the β-catenin and TCF4 protein expression by repressing FOXN3 expression, resulting in the activation of the Wnt/β-catenin signaling pathway, but the activity of the Wnt/β-catenin signaling pathway was inhibited by a miR-574-5p inhibitor or FOXN3 overexpression, which reversed the effect of miR-574-5p. Wound-healing and Transwell assays also showed that miR-574-5p promotes the cell migration and invasion of NPC cells, whereas the promoting effect of miR-574-5p was also reversed by a miR-574-5p inhibitor or FOXN3 overexpression. Collectively, these data suggested that miR-574-5p promotes NPC cell proliferation, migration, and invasion at least partly by targeting the FOXN3/Wnt/β-Catenin signaling pathway.
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