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p38 激活的蛋白激酶信号通路介导的自噬在镉暴露的单巢轮虫褶皱臂尾轮虫中的作用

The role of the p38-activated protein kinase signaling pathway-mediated autophagy in cadmium-exposed monogonont rotifer Brachious koreanus.

作者信息

Kang Hye-Min, Jeong Chang-Bum, Kim Min-Sub, Lee Jin-Sol, Zhou Jiaying, Lee Young Hwan, Kim Duck-Hyun, Moon Eunyoung, Kweon Hee-Seok, Lee Su-Jae, Lee Jae-Seong

机构信息

Department of Biological Science, College of Science, Sungkyunkwan University, Suwon 16419, South Korea.

Department of Biological Science, College of Science, Sungkyunkwan University, Suwon 16419, South Korea; Department of Chemistry, College of Science, Duksung Woman's University, Seoul 01369, South Korea.

出版信息

Aquat Toxicol. 2018 Jan;194:46-56. doi: 10.1016/j.aquatox.2017.11.002. Epub 2017 Nov 10.

DOI:10.1016/j.aquatox.2017.11.002
PMID:29149643
Abstract

Autophagy is a 'self-eating' system that regulates the degradation of cellular components and is involved in various biological processes including survival and development. However, despite its crucial role in organisms, the regulatory mechanism of autophagy remains largely unclear, particularly in invertebrates. In this study, conserved autophagy in the rotifer Brachionus koreanus in response to cadmium (Cd) exposure was verified by measuring acidic vesicle organelles using acridine orange (AO) and neutral red (NR) staining, and by detecting LC3 I/II on Western blot and immunofluorescence. We also demonstrated activation of p38 mitogen-activated protein kinase (MAPK) in response to Cd-induced oxidative stress, leading to the induction of autophagy in B. koreanus. This was further verified by analysis of MAPK protein levels and immunofluorescence of LC3 I/II after treatment with reactive oxygen species (ROS) scavengers and inhibitors specific to MAPKs. We propose a p38 MAPK-mediated regulatory mechanism of autophagy in B. koreanus in response to Cd-induced oxidative stress. This study will contribute to a better understanding of autophagic processes in invertebrates and its modulation by environmental stressors.

摘要

自噬是一种“自我吞噬”系统,可调节细胞成分的降解,并参与包括生存和发育在内的各种生物过程。然而,尽管自噬在生物体中起着至关重要的作用,但其调节机制在很大程度上仍不清楚,尤其是在无脊椎动物中。在本研究中,通过使用吖啶橙(AO)和中性红(NR)染色测量酸性囊泡细胞器,以及通过蛋白质免疫印迹和免疫荧光检测LC3 I/II,验证了轮虫韩国臂尾轮虫(Brachionus koreanus)中对镉(Cd)暴露的保守自噬。我们还证明了p38丝裂原活化蛋白激酶(MAPK)在响应Cd诱导的氧化应激时被激活,从而导致韩国臂尾轮虫中自噬的诱导。在用活性氧(ROS)清除剂和MAPKs特异性抑制剂处理后,通过分析MAPK蛋白水平和LC3 I/II的免疫荧光进一步验证了这一点。我们提出了一种p38 MAPK介导的韩国臂尾轮虫自噬调节机制,以响应Cd诱导的氧化应激。这项研究将有助于更好地理解无脊椎动物中的自噬过程及其受环境应激源的调节。

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