| 内源性CO对内皮素促大鼠主动脉平滑肌细胞增殖及MAPK活性的影响 |
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| 引用本文： | Ou HS,Yan LM,Fu MG,Wang XH,Pang YZ,Su JY,Tang CS. 内源性CO对内皮素促大鼠主动脉平滑肌细胞增殖及MAPK活性的影响[J]. 生理学报, 1999, 51(3): 315-320 |
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| 作者姓名： | Ou HS Yan LM Fu MG Wang XH Pang YZ Su JY Tang CS |
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| 作者单位： | 1. 北京医科大学第一临床医院心血管研究所,北京,100034
2. 衡阳医学院内基诊断学教研室,湖南衡阳市,421001 |
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| 摘 要： | 血红素加氧酶（ｈｅｍｅ ｏｘｙｇｅｎａｓｅ,ＨＯ）是血红素分解代谢过程中的限速酶,它能使细胞内的血红素降解成胆绿素和一氧化碳（ｃａｒｂｏｎｍｏｎｏｘｉｄｅ,ＣＯ）,近来资料表明内源性一氧化碳对生理和病理状态下的血管张力有重要的调节作用,目前尚不不禁内源性ＨＯ／ＣＯ刘否参与平滑肌细胞增殖过程的调节,本实验在体内培养的大鼠主动脉平滑肌细胞模型上,用血色素加氧酶抑制剂卟啉锌－９（ｚｉｎｃ ｐｒｏｔｏｐｏ
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| 关 键 词： | 血色素加氧酶 一氧化碳 血管平滑肌 内皮素 MAPK |
The role of endogenous CO in the regulation of endothelin-induced VSMC proliferation and MAPK activity |
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| Ou H S,Yan L M,Fu M G,Wang X H,Pang Y Z,Su J Y,Tang C S. The role of endogenous CO in the regulation of endothelin-induced VSMC proliferation and MAPK activity[J]. Acta Physiologica Sinica, 1999, 51(3): 315-320 |
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| Authors: | Ou H S Yan L M Fu M G Wang X H Pang Y Z Su J Y Tang C S |
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| Affiliation: | Institute of Vascular Research, First Clinical Hospital, Beijing Medical University, Beijing 100034. |
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| Abstract: | Heme oxygenase (HO) is a rate-limiting enzyme of heme degradation, which converts the cellular heme to bilirubin and carbon monoxide (CO). Recently it is suggested that endogenous CO plays an important role in regulating vascular tone under both physiological and pathological conditions, but it is not clear whether endogenous HO/CO system regulates vascular smooth muscle cell (VSMC) proliferation. In the present study, VMSC 3H-TdR incorporation, mitogen-activated protein kinase (MAPK) activity, HO activity and CO release were determined to study the role of endogenous HO/CO system in regulating the VSMC proliferation induced by endothelin-1 (ET-1) in a cultured system. The results showed that ET-1 increased VSMC 3H-TdR incorporation, MAPK activity, HO activity, and CO release were up-regulated. Pretreatment of HO inhibitor, zinc protoporphyrin-9 (ZnPP-9), increased the ET-1-induced VSMC 3H-TdR incorporation and MAPK activity by 31.8% and 36.6% (P < 0.01, respectively), whereas pretreatment of heme-L-lysinate (HLL), a HO substrate, inhibited these activities. This study demonstrated that up-regulation of VSMC endogenous HO represents a cellular protective response to stress or injury. Inhibition of HO may enhance VSMC proliferation induced by ET-1 in vitro, suggesting that endogenous HO/CO system may be directly involved in the regulation of VSMC proliferation through MAPK signaling pathway. |
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| Keywords: | heme oxygenase carbon monoxide mitogen activated protein kinase vascular smooth muscle cell proliferation |
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