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首页> 外文期刊>Biomaterials Science >miR-96-5p and miR-101-3p as potential intervention targets to rescue TiO2 NP-induced autophagy and migration impairment of human trophoblastic cells
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miR-96-5p and miR-101-3p as potential intervention targets to rescue TiO2 NP-induced autophagy and migration impairment of human trophoblastic cells

机译：mir-96-5p和miR-101-3p作为拯救TiO2 NP诱发的自噬和迁移损伤的潜在干预目标的潜在干预目标

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摘要

Autophagy induced by titanium dioxide nanoparticles (TiO2 NPs) has been realized nowadays, but the underlying mechanisms remain largely unknown. Animal studies have confirmed that autophagy might be an important mechanism to impair placenta development, but the reversal of damage is not clear. Here, we used human HTR-8/SVneo (HTR) cells as a proper model to explore how autophagy is regulated in TiO2 NP-exposed human placenta cells. Our studies showed that TiO2 NPs could enter HTR cells and locate in cytoplasm. Although they did not affect cell viability even under 100 g ml(-1), autophagy was observed and cell migration ability was severely impaired. Further study showed that TiO2 NPs increased the expressions of both miR-96-5p and miR-101-3p and then, they targeted mTOR and decreased the expression of mTOR proteins. In addition, miR-96-5p also targeted Bcl-2 to down-regulate Bcl-2 protein level, which is also a key regulator of autophagy. We proved that when two microRNA inhibitors were added, cell autophagy was, to a greater extent, reversed compared with the result when one inhibitor was added, and the cell migration ability was also reversed to a greater degree. Our studies revealed that TiO2 NPs might impair placenta development via autophagy. Moreover, miR-96-5p as well as miR-101-3p may act as potential targets to reverse TiO2 NP-induced autophagy and placenta dysfunction.
机译：如今已经实现了二氧化钛纳米颗粒（TiO2 NPS）诱导的自噬，但下面的机制仍然很大程度上是未知的。动物研究证实，自噬可能是损害胎盘发展的重要机制，但损坏的逆转尚不清楚。在这里，我们使用人HTR-8 / Svneo（HTR）细胞作为适当模型，以探讨如何在TiO2 NP暴露的人胎盘细胞中调节自噬。我们的研究表明，TiO2 NPS可以进入HTR细胞并定位在细胞质中。虽然它们在100g ml（-1）下不影响细胞活力，但观察到自噬，并且细胞迁移能力严重受损。进一步的研究表明，TiO2 NPS增加了MiR-96-5P和MIR-101-3P的表达，然后，它们靶向MTOR并降低了MTOR蛋白的表达。此外，miR-96-5p还靶向BCL-2至下调BCL-2蛋白质水平，这也是自噬的关键调节器。我们证明，当添加两种微小RNA抑制剂时，细胞自噬在于，在加入一个抑制剂时，细胞自噬相比逆转，并且细胞迁移能力也逆转到更大程度。我们的研究显示，TiO2 NPS可能通过自噬损害胎盘发展。此外，miR-96-5p以及miR-101-3p可以充当反转TiO2 NP诱导的自噬和胎盘功能障碍的潜在靶标。

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  • 来源
    《Biomaterials Science》 |2018年第12期|共11页
  • 作者

    Mao Zhilei; Yao Mengmeng; Li Yaqi; Fu Ziqiang; Li Shushu; Zhang Lina; Zhou Zhu; Tang Qiusha; Han Xiumei; Xia Yankai;

  • 作者单位

    Nanjing Med Univ Changzhou Matern &

    Child Hlth Care Hosp Affiliate Changzhou 213003 Jiangsu Peoples R China;

    Nanjing Med Univ Inst Toxicol State Key Lab Reprod Med Nanjing 211100 Jiangsu Peoples R China;

    Nanjing Med Univ Inst Toxicol State Key Lab Reprod Med Nanjing 211100 Jiangsu Peoples R China;

    Nanjing Med Univ Inst Toxicol State Key Lab Reprod Med Nanjing 211100 Jiangsu Peoples R China;

    Nanjing Med Univ Sch Publ Hlth Minist Educ Key Lab Modern Toxicol Nanjing 211100 Jiangsu Peoples R China;

    Nanjing Med Univ Changzhou Matern &

    Child Hlth Care Hosp Affiliate Changzhou 213003 Jiangsu Peoples R China;

    Univ Pacific Dept Pharmaceut &

    Med Chem Stockton CA 95211 USA;

    Southeast Univ Med Sch Nanjing 210009 Jiangsu Peoples R China;

    Nanjing Med Univ Inst Toxicol State Key Lab Reprod Med Nanjing 211100 Jiangsu Peoples R China;

    Nanjing Med Univ Inst Toxicol State Key Lab Reprod Med Nanjing 211100 Jiangsu Peoples R China;

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  • 正文语种 eng
  • 中图分类 分子生物学;
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