血管光滑肌细胞血红氧酶产生瓜尼利环酶刺激性一氧化碳
N Christodoulides1, W Durante, M H Kroll
1Houston (Tex) Veterans Affairs Medical Center 77030, USA.
Circulation
|May 1, 1995
概括
血管光滑肌细胞 (SMCs) 通过血红氧酶 (HO) 活动产生一氧化碳 (CO). 这种CO刺激了SMC和血小板中的cGMP产生,表明了一种新的信号通路.
科学领域:
- 血管生物学 血管生物学
- 细胞信号传输 细胞信号传输
- 生物化学 生物化学
背景情况:
- 一氧化碳 (CO) 和氧化 (NO) 激活可溶性瓜尼利基环酶,增加细胞内cGMP.
- 血红素氧酶 (HO) 是代谢血红素的酶.
研究的目的:
- 研究血管光滑肌细胞 (SMCs) 内部产生的CO.
- 确定血氧化酶 (HO) 在SMC中的CO生成中的作用.
- 评估SMC衍生的CO对cGMP水平的影响.
主要方法:
- 使用培养的老鼠大动脉SMCs (RASMCs).
- 评估了血氧酶-1 (HO-1) 和血氧酶-2 (HO-2) 的表达.
- RASMCs 用HO-1诱导剂 (血红素,甲) 进行治疗.
- 测量了RASMC和并存血小板中的cGMP水平.
- 使用了血氧酶抑制剂 (原氨酸IX).
主要成果:
- 拉斯姆克表达了HO-1和HO-2.
- 诱导HO-1增加了RASMC和血小板中的cGMP.
- 由RASMCs诱导的CO产生增加了血小板cGMP.
- NO合成酶活动与观察到的cGMP增加无关.
- 血液氧化酶抑制逆转了cGMP的升高.
结论:
- 血管SMC具有构成性和诱导性血红素氧酶活性.
- SMCs产生CO,刺激SMC和血小板中的甘基酶.
- 这突出了血管细胞中一种新的内源性CO介导信号通路.
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