通过gp130在心脏肌细胞中的白血病抑制因子激活JAK-STAT和MAP激酶
K Kunisada1, H Hirota, Y Fujio
1Department of Medicine III, Osaka University Medical School, Japan.
Circulation
|November 15, 1996
概括
白血病抑制因子 (LIF) 激活了心脏肌细胞中的Janus激酶信号转换器和转录激活器 (JAK-STAT) 和基激活蛋白激酶 (MAPK) 途径. 这种gp130介导的信号传输迅速发生,无论是体外还是体外.
科学领域:
- 心血管生物学 心血管生物学
- 细胞信号传递 细胞信号传递
- 分子医学是分子医学.
背景情况:
- 介素-6 (IL-6) 相关的细胞因子利用gp130进行信号传导.
- gp130的两个主要下游途径是Janus激酶信号转换器和转录激活器 (JAK-STAT) 和Ras-mitogen激活蛋白激酶 (MAPK) 途径.
- 这些通路在心脏肌细胞中的存在和激活以前没有被描述.
研究的目的:
- 研究心脏肌细胞中gp130下游的JAK-STAT和MAPK信号通路的激活.
- 确定白血病抑制因子 (LIF) 在激活心脏细胞中这些通路中的作用.
主要方法:
- 新生小鼠心肌细胞被LIF刺激.
- 蛋白质激活被评估使用免疫沉和西方抹杀的色胺.
- 使用抗gp130抗体研究了信号通路的抑制.
- 在体内研究涉及成年小鼠静脉注射LIF,随后进行心脏组织分析.
主要成果:
- 在心脏肌细胞中,LIF刺激诱导了gp130,JAK1和STAT3的铁酸化.
- 线素激活蛋白激酶 (MAPKs) 在LIF暴露后5分钟内显示出最大的激活.
- 反gp130抗体阻断了LIF诱导的JAK1,STAT3和MAPKs的激活.
- 在体内,LIF治疗激活了成年小鼠心中的gp130,STAT3和MAPK.
结论:
- 心脏肌细胞具有gp130.0.下游的JAK-STAT和MAPK信号通路.
- 在心脏肌细胞中,LIF迅速激活这些通路,无论是体外还是体外.
- 激活gp130代表了心脏肌细胞内的新型信号机制.
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