オバラ　チズカ   Obara Chizuka   小原　千寿香    所属   東邦大学  理学部 生物学科    職種   博士研究員
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Radiation increases the cellular uptake of exosomes through CD29/CD81 complex formation
掲載誌名	正式名：BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS ISSNコード：0006-291X/1090-2104
出版社	ACADEMIC PRESS INC ELSEVIER SCIENCE
巻・号・頁	446(4),pp.1165-1171
著者・共著者	Masaharu Hazawa,Kenichi Tomiyama,Ai Saotome-Nakamura,Chizuka Obara,Takeshi Yasuda,Takaya Gotoh,Izumi Tanaka,Haruko Yakumaru,Hiroshi Ishihara,Katsushi Tajima
発行年月	2014/04
概要	Exosomes mediate intercellular communication, and mesenchymal stem cells (MSC) or their secreted exosomes affect a number of pathophysiologic states. Clinical applications of MSC and exosomes are increasingly anticipated. Radiation therapy is the main therapeutic tool for a number of various conditions. The cellular uptake mechanisms of exosomes and the effects of radiation on exosome-cell interactions are crucial, but they are not well understood. Here we examined the basic mechanisms and effects of radiation on exosome uptake processes in MSC. Radiation increased the cellular uptake of exosomes. Radiation markedly enhanced the initial cellular attachment to exosomes and induced the colocalization of integrin CD29 and tetraspanin CD81 on the cell surface without affecting their expression levels. Exosomes dominantly bound to the CD29/CD81 complex. Knockdown of CD29 completely inhibited the radiation-induced uptake, and additional or single knockdown of CD81 inhibited basal uptake as well as the increase in radiation-induced uptake. We also examined possible exosome uptake processes affected by radiation. Radiation-induced changes did not involve dynamin2, reactive oxygen species, or their evoked p38 mitogen-activated protein kinase-dependent endocytic or pinocytic pathways. Radiation increased the cellular uptake of exosomes through CD29/CD81 complex formation. These findings provide essential basic insights for potential therapeutic applications of exosomes or MSC in combination with radiation. (C) 2014 Elsevier Inc. All rights reserved.
DOI	10.1016/j.bbrc.2014.03.067
PMID	24667602