埃皮瑞古林作为一个主要的自/对因子,从ERK和p38MAPK激活的血管光滑肌细胞中释放出来
Masanori Takahashi1, Ken'ichiro Hayashi, Kenji Yoshida
1Department of Neuroscience, Osaka University Graduate School of Medicine (D13), 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Circulation
|October 29, 2003
概括
埃皮瑞古林被确定为血管光滑肌细胞 (VSMC) 释放的关键因子,促进它们的脱差. 这一发现揭示了诸如动脉样硬化等血管改造过程.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 心血管研究研究心血管研究
背景情况:
- ERK和p38MAPK的协调激活对于光滑肌肉细胞 (SMC) 不分化至关重要.
- 内脏SMC分泌的因素诱导邻近SMC的脱差.
- 从血管SMCs (VSMCs) 的特定脱差因子仍然未确定.
研究的目的:
- 确定由VSMCs分泌的脱差因子.
- 调查已识别的因素在VSMC脱差和血管改造中的作用.
主要方法:
- 从激活的VSMC中分化条件介质.
- 鉴定epiregulin作为一个关键因素.
- 对埃皮瑞古林诱导的信号通路 (ERK,p38MAPK) 的分析.
- 使用RT-PCR和免疫组织学评估人类和老鼠动脉中的epiregulin表达.
主要成果:
- 埃皮瑞古林被确定为VSMC脱差的主要自克林/克林因子.
- 经由ERK和p38MAPK激活的介导而引起的Epiregulin脱差.
- Lysophosphatidic 酸和 PDGF-BB 调高了埃皮瑞古林的表达.
- 埃皮瑞古林在动脉样硬化和损伤的动脉中表达,与VSMC表型调制相关.
结论:
- 埃皮雷古林是由VSMCs在异位性条件下释放出来的.
- 埃皮瑞古林在VSMC分离过程中起着显著的自克林/克林因子的作用.
- 埃皮瑞古林可能在血管改造的进展中发挥作用,包括动脉样硬化.
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