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Modulation of normal human skin fibroblasts responses to ionizing radiations by gap junction

https://repo.qst.go.jp/records/70868
https://repo.qst.go.jp/records/70868
15b8d945-e219-417d-b826-c305a99bd692
Item type 会議発表用資料 / Presentation(1)
公開日 2012-09-10
タイトル
タイトル Modulation of normal human skin fibroblasts responses to ionizing radiations by gap junction
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_c94f
資源タイプ conference object
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Autsavapromporn, Narongchai

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WEKO 696357

Autsavapromporn, Narongchai

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Suzuki, Masao

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WEKO 696358

Suzuki, Masao

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Hua, Liu Cui

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WEKO 696359

Hua, Liu Cui

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Uchihori, Yukio

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WEKO 696360

Uchihori, Yukio

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K, Hei Tom

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WEKO 696361

K, Hei Tom

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Azzam, Edouard

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WEKO 696362

Azzam, Edouard

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Murakami, Takeshi

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WEKO 696363

Murakami, Takeshi

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アッサワプロンポーン ナロンチャイ

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WEKO 696364

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鈴木 雅雄

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劉 翠華

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内堀 幸夫

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村上 健

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抄録
内容記述タイプ Abstract
内容記述 Understanding the biological effects of different types of ionizing radiation (IR) is essential for cancer therapy. Here, we focused on the role of gap junction intercellular communication (GJIC) modulating the repair of potentially lethal damage (PLDR) and micronuclei formation in cells exposed to low- or high-linear energy transfer (LET) IR, by which every cell is traversed by IR track. Confluent cells were exposed in the presence or absence of gap junction inhibitor to X rays (LET-1.7keV/um), carbon ions (LET-76keV/um), silicon ions (LET-113keV/um) or iron ions (LET-400keV/um) that result in isosurvival levels. They were incubated for various times at 37oC. As expected, high-LET IR were more effective than low-LET IR at inducing of cell killing and DNA damage, shortly after irradiation. However, maintaining cells in the confluent state for various times resulted in PLDR coupled with a reduction in DNA damage, occurred only in cells exposed to low-LET IR, but not in those exposed to high-LET IR. Interestingly, inhibition of GJIC significantly enhanced cell survival and a reduction in DNA damage in cells exposed to high-LET IR but not in low-LET IR. Overall, these results show that LET and GJIC play an important role of the propagation of stressful effects in among irradiated cells exposed to high-LET IR and that GJIC has only minimal effect on PLDR and induction of DNA damage following low-LET IR. This finding opens the new approaches in cancer treatment.
会議概要(会議名, 開催地, 会期, 主催者等)
内容記述タイプ Other
内容記述 日本放射線影響学会第55回大会
発表年月日
日付 2012-09-08
日付タイプ Issued
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