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  1. H-1. がん進展制御研究所
  2. h-1 10. 学術雑誌掲載論文
  3. 1. 査読済論文

Attenuated liver tumor formation in the absence of CCR2 with a concomitant reduction in the accumulation of hepatic stellate cells, macrophages and neovascularization

http://hdl.handle.net/2297/6665
http://hdl.handle.net/2297/6665
04e8b8f1-fbb0-4ddd-a7ee-609586da95fc
名前 / ファイル ライセンス アクション
CA-PR-MUKAIDA-N-335.pdf CA-PR-MUKAIDA-N-335.pdf (1.8 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2017-10-05
タイトル
タイトル Attenuated liver tumor formation in the absence of CCR2 with a concomitant reduction in the accumulation of hepatic stellate cells, macrophages and neovascularization
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
著者 Yang, Xiaoqin

× Yang, Xiaoqin

WEKO 47520

Yang, Xiaoqin

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Lu, Peirong

× Lu, Peirong

WEKO 47521

Lu, Peirong

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Ishida, Yuko

× Ishida, Yuko

WEKO 47522

Ishida, Yuko

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Kuziel, William A.

× Kuziel, William A.

WEKO 47523

Kuziel, William A.

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Fujii, Chifumi

× Fujii, Chifumi

WEKO 17028
研究者番号 10361982

Fujii, Chifumi

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Mukaida, Naofumi

× Mukaida, Naofumi

WEKO 49
e-Rad 30182067
金沢大学研究者情報 30182067
研究者番号 30182067

Mukaida, Naofumi

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提供者所属
内容記述タイプ Other
内容記述 金沢大学がん研究所がん病態制御
書誌情報 International Journal of Cancer

巻 118, 号 2, p. 335-345, 発行日 2006-11-15
ISSN
収録物識別子タイプ ISSN
収録物識別子 1097-0215
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 https://doi.org/10.1002/ijc.21371
出版者
出版者 Wiley-Liss
抄録
内容記述タイプ Abstract
内容記述 The liver parenchyma is populated by hepatocytes and several nonparenchymal cell types, including Kupffer cells and hepatic stellate cells. Both Kupffer cells and hepatic stellate cells are responsive to the chemokine CCL2, but the precise roles of CCL2 and these cells in liver tumor formation remain undefined. Hence, we investigated the effects of the lack of the major CCL2 receptor, CCR2, on liver tumor formation induced by intraportal injection of the murine colon adenocarcinoma cell line, colon 26. Wild-type mice showed macroscopic tumor foci in the liver 10 days after injection of colon 26 cells. After 10 days, CCL2 proteins were detected predominantly in tumor cells, coincident with increased intratumoral macrophage and hepatic stellate cell numbers. Although tumor formation occurred at similar rates in wild-type and CCR2-deficient mice up to 10 days after tumor cell injection, the number and size of tumor foci were significantly attenuated in CCR2-deficient mice relative to wild-type mice thereafter. Moreover, neovascularization and matrix metalloproteinase 2 expression were diminished in CCR2-deficient mice with a concomitant reduction in the accumulation of macrophages and hepatic stellate cells. Furthermore, matrix metalloproteinase 2 was detected predominantly in hepatic stellate cells but not in macrophages. We provided the first definitive evidence that the absence of CCR2-mediated signals can reduce the trafficking of hepatic stellate cells, a main source of matrix metalloproteinase 2, and consequently can diminish neovascularization during liver tumor formation. © 2005 Wiley-Liss, Inc.
著者版フラグ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
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