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Insulin-like growth factor-I induces reactive oxygen species production and cell migration through Nox4 and Rac1 in vascular smooth muscle cells
文献类型：期刊论文
| 作者 | Meng, Dan; Lv, Dan-Dan; Fang, Jing（方靖） |
| 刊名 | CARDIOVASCULAR RESEARCH
 |
| 出版日期 | 2008 |
| 卷号 | 80期号:2页码:299-308 |
| 关键词 | Vascular smooth muscle cells Insulin-like growth factor-I Reactive oxygen species Nox4 Rac1 |
| 通讯作者 | Fang, J (reprint author), Chinese Acad Sci, Key Lab Nutr & Metab, Inst Nutr Sci, Shanghai Inst Biol Sci, 294 Tai Yuan Rd, Shanghai 200031, Peoples R China. |
| 英文摘要 | Aims We showed previously that insulin-like growth factor-I (IGF-I)-induced vascular smooth muscle cells (VSMCs) proliferation through the production of reactive oxygen species (ROS). However, how IGF-I-induced ROS was unknown. The aim of this study is to investigate the mechanisms by which IGF-I induces ROS production in VSMCs. Methods results Reverse transcription-PCR, real-time PCR, immunoblotting, and confocal microscopic image analysis were employed to determine protein expression, small Rho-GTPase Rac1 activation, and ROS production. Inhibition of NADPH oxidase 4 (Nox4) or Rac1 was performed by means of siRNA technology. Inhibition of Rac1 activity was accomplished using dominant-negative form of Rac1 (N17Rac1) plasmid. VSMCs from Sprague-Dawley rat thoracic aortas were used in this work.IGF-I enhanced ROS production in rat VSMCs. IGF-I increased the protein level of Nox4 but had little effect on its mRNA level. IGF-I induced the activation of Rac1. Either knockdown of Nox4 or inactivation of Rac1 impaired IGF-I-induced ROS. Over-expression of Nox4 increased NADPH oxidase activity, which was not influenced by inactivation of Rac1. Neither over-expression nor knockdown of Rac1 influenced Nox4 expression. Knockdown of Nox4 did not affect IGF-I-induced activation of Rac1. IGF-I increased matrix metalloproteinase (MMP)-2 and 9 activity and promoted VSMC migration, which was inhibited by knockdown of Nox4 and inactivation of Rac1. Conclusion Our results suggest that Nox4 and Rac1 mediate IGF-I-induced ROS production and cell migration in VSMCs and that Nox4 is not regulated by Rac1. |
| 类目[WOS] | Cardiac & Cardiovascular Systems |
| 研究领域[WOS] | Cardiovascular System & Cardiology |
| 关键词[WOS] | NAD(P)H OXIDASE ; NADPH OXIDASE ; PHOSPHATIDYLINOSITOL 3-KINASE ; FACTOR-RECEPTOR ; UP-REGULATION ; IGF-I ; PROLIFERATION ; PROTEINS ; ATHEROSCLEROSIS ; EXPRESSION |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000260134700018 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/353]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所_营养与癌症研究组 |
| 推荐引用方式 GB/T 7714 | Meng, Dan,Lv, Dan-Dan,Fang, Jing. Insulin-like growth factor-I induces reactive oxygen species production and cell migration through Nox4 and Rac1 in vascular smooth muscle cells[J]. CARDIOVASCULAR RESEARCH,2008,80(2):299-308. |
| APA | Meng, Dan,Lv, Dan-Dan,&Fang, Jing.(2008).Insulin-like growth factor-I induces reactive oxygen species production and cell migration through Nox4 and Rac1 in vascular smooth muscle cells.CARDIOVASCULAR RESEARCH,80(2),299-308. |
| MLA | Meng, Dan,et al."Insulin-like growth factor-I induces reactive oxygen species production and cell migration through Nox4 and Rac1 in vascular smooth muscle cells".CARDIOVASCULAR RESEARCH 80.2(2008):299-308. |
入库方式： OAI收割
来源：上海营养与健康研究所
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