研究者業績

久米 晃啓

クメ アキヒロ  (Akihiro Kume)

基本情報

所属
自治医科大学 附属病院臨床研究センター企画開発部 教授
学位
博士(医学)(東北大学)

J-GLOBAL ID
200901072254016208
researchmap会員ID
1000193248

論文

 124
  • Yuji Kashiwakura, Kazuhiro Endo, Atsushi Ugajin, Tomohiro Kikuchi, Shuji Hishikawa, Hitoyasu Nakamura, Yuko Katakai, Nemekhbayar Baatartsogt, Takafumi Hiramoto, Morisada Hayakawa, Nobuhiko Kamoshita, Shoji Yamazaki, Akihiro Kume, Harushi Mori, Naohiro Sata, Yoichi Sakata, Shin-ichi Muramatsu, Tsukasa Ohmori
    Molecular Therapy - Methods & Clinical Development 2023年8月  
  • 柏倉 裕志, 遠藤 和洋, 宇賀神 敦, 菊地 智博, 菱川 修司, 中村 仁康, 片貝 祐子, Nemekhbayar Baatartsogt, 平本 貴史, 早川 盛禎, 鴨下 信彦, 山崎 晶司, 久米 晃啓, 森 墾, 佐田 尚宏, 坂田 洋一, 村松 慎一, 大森 司
    日本血栓止血学会誌 34(2) 240-240 2023年5月  
  • Teruhide Yamaguchi, Eriko Uchida, Takashi Okada, Keiya Ozawa, Masafumi Onodera, Akihiro Kume, Takashi Shimada, Satoru Takahashi, Kenzaburo Tani, Yasutomo Nasu, Tomoji Mashimo, Hiroyuki Mizuguchi, Kohnosuke Mitani, Kazushige Maki
    Human gene therapy 31(19-20) 1043-1053 2020年10月  
    The development of genome-editing technology could lead to breakthrough gene therapy. Genome editing has made it possible to easily knock out or modify a target gene, while current gene therapy using a virus vector or plasmid hampering modification with respect to gene replacement therapies. Clinical development using these genome-editing tools is progressing rapidly. However, it is also becoming clear that there is a possibility of unintended gene sequence modification or deletion, or the insertion of undesired genes, or the selection of cells with abnormalities in the cancer suppressor gene p53; these unwanted actions are not possible with current gene therapy. The Science Board of the Pharmaceuticals and Medical Devices Agency of Japan has compiled a report on the expected aspects of such genome-editing technology and the risks associated with it. This article summarizes the history of that discussion and compares the key concepts with information provided by other regulatory authorities.
  • Miyata S, Tominaga K, Sakashita E, Urabe M, Onuki Y, Gomi A, Yamaguchi T, Mieno M, Mizukami H, Kume A, Ozawa K, Watanabe E, Kawai K, Endo H
    Scientific reports 9(1) 9787 2019年7月  査読有り
  • Fumio Kurosaki, Ryosuke Uchibori, Yoshihide Sehara, Yasushi Saga, Masashi Urabe, Hiroaki Mizukami, Koichi Hagiwara, Akihiro Kume
    Human gene therapy 29(11) 1242-1251 2018年11月  査読有り
    Idiopathic pulmonary fibrosis (IPF) is a fibroproliferative disorder with limited therapeutic options. An aberrant wound healing process in response to repetitive lung injury has been suggested for its pathogenesis, and a number of cytokines including transforming growth factor β1 play pivotal roles in the induction and progression of fibrosis. Thus, the regulation of these pro-inflammatory conditions may reduce the progression of IPF and ameliorate its symptoms in patients. Interleukin-10 (IL-10), a pleiotropic cytokine, exerts anti-inflammatory and anti-fibrotic effects in numerous biological settings. In the present study, we investigated the preventive effects of IL-10 on bleomycin-induced pulmonary fibrosis in mice with the continuous expression of this cytokine via an adeno-associated virus serotype 6 vector. Mice were administered the adeno-associated virus serotype 6 vector encoding mouse IL-10 by intratracheal injection, and osmotic minipumps containing bleomycin were subcutaneously implanted seven days later. Lung histology and the expression levels of pro-inflammatory cytokines and fibrogenic cytokines were then analyzed. In mice exhibiting persistent IL-10 expression on day 35, the number of infiltrated inflammatory cells and the development of fibrosis in lung tissues were significantly reduced. Increases in transforming growth factor β1 and decreases in IFN-γ were also suppressed in treated animals, with changes in these cytokines playing important roles in the pathogenesis of pulmonary fibrosis. Furthermore, IL-10 significantly improved survival in bleomycin-induced mice. Our results provide insights into the potential benefit of the anti-fibrotic effects of IL-10 as a novel therapeutic approach for IPF.

MISC

 173

共同研究・競争的資金等の研究課題

 27