Toxicity of Graphene Oxide in Nematodes with a Deficit in the Epidermal Barrier Caused by RNA Interference Knockdown of unc-52

被引:15
作者
Ding, Xuecheng [1 ,2 ]
Rui, Qi [1 ]
Zhao, Yunli [3 ]
Shao, Huimin [2 ]
Yin, Yiping [2 ]
Wu, Qiuli [2 ]
Wang, Dayong [2 ]
机构
[1] Nanjing Agr Univ, Coll Life Sci, Nanjing 210095, Jiangsu, Peoples R China
[2] Southeast Univ, Med Sch, Minist Educ, Key Lab Environm Med Engn, Nanjing 210009, Jiangsu, Peoples R China
[3] Bengbu Med Coll, Dept Prevent Med, Bengbu 233030, Peoples R China
来源
ENVIRONMENTAL SCIENCE & TECHNOLOGY LETTERS | 2018年 / 5卷 / 11期
基金
中国国家自然科学基金;
关键词
CAENORHABDITIS-ELEGANS; NANOPOLYSTYRENE PARTICLES; COMPLEX PATTERNS; OXIDATIVE STRESS; SPLICE VARIANTS; MOLECULAR-BASIS; CELL ADHESION; NANOPARTICLES; PROTEIN; DAMAGE;
D O I
10.1021/acs.estlett.8b00473
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
The epidermal barrier is important for the defense of environmental organisms against the damage from engineered nanomaterials (ENMs). We employed Caenorhabditis elegans to examine the possible influence of a deficit in the epidermal barrier caused by RNA interference (RNAi) knockdown of unc-52 encoding a perlecan protein on the toxicity of graphene oxide (GO). Epidermal RNAi knockdown of unc-52 caused a functional deficit in the epidermal barrier and susceptibility to GO toxicity. Epidermal knockdown of unc-52 decreased the level of expression of fbl-1 encoding a membrane protein fibulin and sax-7 encoding a cell adhesion receptor, and epidermal knockdown of fbl-1 or sax-7 also resulted in a functional deficit in the epidermal barrier and susceptibility to GO toxicity. Additionally, epidermal knockdown of unc-52 inhibited expression of cnc-2 and prx-11 encoding two antimicrobial proteins, and epidermal knockdown of cnc-2 or prx-11 could strengthen the GO toxicity in fbl-1(RNAi) or sax-7(RNAi) nematodes. Our data further highlight the important function of the epidermal barrier against toxicity of environmental ENMs.
引用
收藏
页码:622 / 628
页数:13
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