Quantum dots induced monocyte chemotactic protein-1 expression via MyD88-dependent Toll-like receptor signaling pathways in macrophages

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Title:	Quantum dots induced monocyte chemotactic protein-1 expression via MyD88-dependent Toll-like receptor signaling pathways in macrophages
Authors:	羅月霞;Ho, Chia-Chi;Luo, Yueh-Hsia;Chuang, Tsung-Hsien;Yang, Chung-Shi;Ling, Yong-Chien;Lin, Pinpin
Contributors:	生醫理工學院生命科學系
Keywords:	Animals;Cell Line;Chemokine CCL2 - biosynthesis;Chemokine CCL2 - genetics;chemokines;Chromogenic Compounds - pharmacology;Emergency;endocytosis;Gene Expression Regulation - drug effects;Immune systems;Inflammation;Inhibitors;lungs;macrophages;Macrophages - metabolism;MCP-1;Mice;MyD88;Myeloid Differentiation Factor 88 - biosynthesis;Myeloid Differentiation Factor 88 - physiology;Nanostructure;NF-κB;Particle Size;Pathways;Proteins;QD705;Quantum Dots;Semiconductors;signal transduction;Signal Transduction - drug effects;Signal Transduction - physiology;small interfering RNA;Surface chemistry;TLRs;Toll-like receptors;Toll-Like Receptors - physiology;toxicology;transcription factor NF-kappa B
Date:	2013-06-07
Issue Date:	2026-04-23 11:13:41 (UTC+8)
Publisher:	Ireland: Elsevier Ireland Ltd
Abstract:	摘要： Quantum dots (QDs) are nano-sized semiconductors. Previously, intratracheal instillation of QD705s induces persistent inflammation in mouse lungs. In our present study, QD705-COOH and QD705-PEG activated NF-κB and increased monocyte chemotactic protein-1 (MCP-1) expression in macrophages RAW264.7 via MyD88 dependent Toll-like receptor (TLR) signaling pathways. MyD88 is an adapter protein for most TLRs to activate NF-κB. Silencing expression of MyD88 or p65 with siRNA or co-treatment with a NF-κB inhibitor tremendously abolished QD705s-induced NF-κB activity and MCP-1 expression. The involved TLRs might locate either on the cell surface or inside of cells. Co-treatment with a TLR4 inhibitor completely prevented MCP-1 induction by QD705-PEG. Nevertheless, QD705-COOH readily entered cells, and co-treatment with either inhibitors of endocytosis or intracellular TLRs prevented MCP-1 induction. These findings indicate that, depending on their surface modification, OD705s activate MyD88 dependent-TLRs at the surface or inside of the cells, which is an important mechanism for nanoparticles-induced inflammatory responses. But other MyD88-independent pathways may also involve in these responses. 其他題名： Toxicology 出版者： Ireland: Elsevier Ireland Ltd 出版日期： 2013-06-07 出處： Toxicology, 2013-06, Vol.308, p.1-9 版權： 2013 Elsevier Ireland Ltd 版權： Elsevier Ireland Ltd 版權： Copyright © 2013 Elsevier Ireland Ltd. All rights reserved. 識別號： ISSN: 0300-483X 識別號： ISSN: 1879-3185 識別號： EISSN: 1879-3185 識別號： DOI: 10.1016/j.tox.2013.03.003 識別號： PMID: 23499856
Appears in Collections:	[Department of Life Science] journal & Dissertation

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