RETRACTED ARTICLE: MiR-106a facilitates the sensorineural hearing loss induced by oxidative stress by targeting connexin-43

We, the Editors and Publisher of the journal <i>Bioengineered</i>, have retracted the following article from publication. Ding, L., &amp; Wang, J. (2022). MiR-106a facilitates the sensorineural hearing loss induced by oxidative stress by targeting connexin-43. <i>Bioengineered</i>, 13(6), 14080–14093. https://doi.org/10.1080/21655979.2022.2071021 Since publication, significant concerns have been raised by a third party about the integrity of the data and reported results in the article. When approached for an explanation, the authors did not respond to our queries and so these serious concerns remain unaddressed. As verifying the validity of published work is core to the integrity of the scholarly record, we are therefore retracting the article. The authors have been informed of this decision. We have been informed in our decision-making by our policy on publishing ethics and integrity and COPE guidelines. The retracted article will remain online to maintain the scholarly record and will be digitally watermarked on each page as ‘Retracted’.

感音神经性耳聋（sensorineural hearing loss, SNHL）是氨基糖苷类抗菌药物（aminoglycoside antibacterial drugs，如庆大霉素（gentamicin））过度使用后常见的临床不良反应。近期研究证实，氧化应激（oxidative stress）是感音神经性耳聋的重要诱因，且该过程与连接蛋白-43（connexin-43）的表达下调密切相关。MicroRNA-106a（miR-106a）已被证实可调控连接蛋白-43的表达。本研究旨在探讨miR-106a是否在感音神经性耳聋的发生发展中发挥关键介导作用。
首先，研究人员在感音神经性耳聋患者的外周血样本中观察到miR-106a表达上调。实验采用葡萄糖氧化酶（glucose oxidase, GO）诱导分离的大鼠耳蜗边缘细胞（marginal cells, MCs）产生氧化损伤，随后转染miR-106a抑制剂。结果发现，葡萄糖氧化酶刺激所致的耳蜗边缘细胞增殖能力下降、凋亡增加及氧化应激激活，可被miR-106a抑制剂显著逆转，同时伴随连接蛋白-43表达上调。通过双荧光素酶报告基因实验（dual luciferase gene reporter assay），研究人员预测并验证了miR-106a与连接蛋白-43之间的靶向调控关系。进一步实验显示，敲低连接蛋白-43可完全消除miR-106a抑制剂对葡萄糖氧化酶处理后的耳蜗边缘细胞增殖、凋亡及氧化应激的调控作用。
此外，研究采用庆大霉素构建大鼠感音神经性耳聋模型，随后分别给予antagomir-106a单独治疗，以及antagomir-106a联合连接蛋白-43抑制剂甘珀酸（carbenoxolone）治疗。结果显示，antagomir-106a治疗可减轻感音神经性耳聋大鼠的耳蜗组织病理损伤、减少细胞凋亡并改善氧化应激状态，而甘珀酸联合给药可显著逆转上述保护效应。
综上，miR-106a通过靶向调控连接蛋白-43，参与氧化应激诱导的感音神经性耳聋的发生发展。