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Cu/ZnSOD and VEGF rescue endothelial damage caused by radiation
https://repo.qst.go.jp/records/69004
https://repo.qst.go.jp/records/6900472a02463-e129-4ae7-933f-0e011b831bfc
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2007-07-04 | |||||
| タイトル | ||||||
| タイトル | Cu/ZnSOD and VEGF rescue endothelial damage caused by radiation | |||||
| 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 |
Tominaga, Takako
× Tominaga, Takako× Akashi, Makoto× et.al× 富永 隆子× 明石 真言 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | The balance between survival and cell death of vascular endothelial cells is regulated by a homeostatic mechanism. This homeostatic mechanism is deregulated by exposure to radiation. It is known that vascular endothelium within the intestinal mucosa is the actual target of radiation damage, with stem cell dysfunction as a consequence in gastrointestinal (GI) tract damage by radiation. Moreover, endothelium is also a principal target for radiation injury to lung, brain, and skin. Thus, vascular damage is a key mechanism in radiation injuries and the vascular endothelial cell death and proliferation are the primary lesion leading to stem cell dysfunction. However, little is known about treatment of radiation-induced vascular damage. We examined the effects of vascular endothelial growth factor (VEGF) and cupper/zinc superoxide dismutase (Cu/ZnSOD) on cell growth in radiation using human primary umbilical vein endothelial cells (HUVEC). These cells were irradiated by various doses of -rays. Studies of cell growth and proliferation by WST1 analyses and viable cell numbers showed that radiation suppressed the cell growth in a dose dependent manner. Flwocytometric analysis found that treatment with an inhibitor of the extracellular signal regulated kinase 1/2 (ERK1/2) pathway blocked the apoptosis induced by radiation with concomitantly blocking phosphorylation of ERK1/2, but culturing with an inhibitor of p38 mitogen-activated protein kinase (p38MAPK) did not affect the apoptosis in these cells. These results suggest that the ERK1/2 pathway promotes cell survival in these cells. Moreover, assays of WST1 showed that treatment of these cells with VEGF or Cu/ZnSOD rescued the cell growth suppression before and also after irradiation and both factors activated the phosphorylation of ERK1/2 in irradiated cells. Thus, our results indicate that VEGF and Cu/ZnSOD may be candidates of therapeutic agents for radiation-induced injury by radiation. | |||||
| 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 | Annual meeting 2007 | |||||
| 発表年月日 | ||||||
| 日付 | 2007-04-18 | |||||
| 日付タイプ | Issued | |||||
