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血管内皮生长因子对培养内皮细胞合成一氧化氮的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2002年第3期
页码:
186-188
栏目:
实验研究
出版日期:
2002-05-01

文章信息/Info

Title:
The effect of vascular endothelial growth factor on nitric oxide release from human umbilical vein endotheial cell
作者:
郝亚荣;  李庚山;  李建军;  王　晶;  赵智深;  赵志明
武汉大学人民医院心内科, 湖北 武汉 430060
Author(s):
HAO Ya-rong ; LI Geng-shan; LI Jian-jun; WANG Jing ;  ZHAO Zhi-shen;  ZHAO Zhi-ming
Department of cardiology, Renmin Hospital of Wuhan University,Wuhan,Hubei 430060, China
关键词:
血管内皮生长因子;  内皮细胞;  一氧化氮
Keywords:
vascular endothelial growth factor;  endothelial cell;  nitric oxide
分类号:
Q593.3
DOI:
-
文献标识码:
A
摘要:
目的 探讨血管内皮生长因子(VEGF)/血管渗透因子(VPF)对内皮细胞(EC)分泌一氧化氮(NO)的影响。方法 将培养的人脐静脉内皮细胞(HUVEC)随机分为6组(n=6/组):①正常对照组;②VEGF 1 ng/ml;③VEGF 10ng/ml;④VEGF 100 ng/ml;⑤低氧组;⑥低氧组+VEGF 100 ng/ml。采用硝酸还原酶法测定培养液中的NO2-,NO3-的含量以反映NO水平。结果 VEGF促进正常EC分泌NO,在一定浓度范围内呈剂量依赖性;低氧损伤EC,使其分泌NO减少;VEGF 100 ng/ml预处理可保护EC免受低氧损害,保持正常分泌NO的功能。结论 VEGF能够调节EC的功能,为其促血管形成作用中EC分裂、增殖、迁移奠定物质基础。
Abstract:
AIM To study the effect of vascular endothelial growth factor(VEGF)/vascular permeability factor(VPF) on nitric oxide(NO) release from human umbilical vein endothelial cell (HUVEC).METHODS The cultured HUVEC were devided into 6 groups:①Control;②VEGF 1 ng/ml;③VEGF 10 ng/ml;④VEGF 100 ng/ml;⑤Hypoxia;⑥Hypoxia+VEGF 100 ng/ml. The medium was collected to test NO content by optical density.RESULTS VEGF promoted endothelial cell (EC) secreting NO and was dose-dependent. Hypoxia damaged EC and decreased NO release. VEGF preconditioning protected EC from injuring by hypoxia.CONCLUSION VEGF modulates the function of EC.

参考文献/References

[1] Kuwabara K,Ogawa S,Matsumoto M,et al. Hypoxia-mediated induction of acid/basic fibroblast growth factor and platelet derived growth factor in mononuclear phagocytes stimulates growth of hypoxic endothelial cells[J].Proc Natl Acad Sci USA,1995,92:4606-6910.

[2] De Vries C,Escobedo JA,Ueno H,et al. The fms-like tyrosine kinase, a receptor for vascular endothelial growth factor[J].Sciencee,1992,255:989-991.

[3] Millauer B,Vizigmann-voos S,Martinez R,et al. High affinity VEGF binding and developmental expression suggest Flk-1 as major regulator of vasculogenesis and angiogenesis[J].Cell,1993,72:835-846.

[4] Ku DD,Zaleski JK,Liu S,et al. Vascular endothelial growth factor induces EDRF-dependent relaxation in coronary arteries [J].Am J Physiol,1993,265:H586-H592.

[5] Zee R,Murohara T,Luo Z,et al. Vascular endothelial growth factor/vascular permeability factor augments nitric oxide release from quiescent rabbit and human vascular endothelium[J].Circulation,1997,95:1030-1037.

[6] Peters KG,deVries C,Williams LT,et al. Vascular endothelial growth factor receptor expression during embryogenesis and tissue repair suggests a role in endothelial differentiation and blood vessel growth[J].Proc Natl Acad Sci USA,1993,90:8915-8919.

[7] Jakeman LB,Winer J,Bennett GL,et al. Binding sites for vascular endothelial growth factor are localized on endothelial cells in adult rat tissues[J].J Clin Invest,1992,89:244-253.

[8] Alon T,Hemo I,Itin A,et al. Vascular endothelial growth factor acts as a survival factor for newly formed retinal vessels and has implications for retinopathy of prematurity[J].Nat Med,1995,1:1024-1028.

[9] Shifren JL,Doldi N,Ferrara N,et al. In the human fetus,vascular endothelial growth factor is expressed in epithelial cells and myocytes,but not vascular endothelium:implications for mode of action[J].J Clin Endocrinol Metab,1994,79:316-322.

[10]De Meyer GRY,Bult H,Ustunes L,et al. Effect of nitric oxide donors in neointima formation and vascular reactivity in the collared carotid artery of rabbits[J].J Cardiovasc Pharmacol,1995,26:272-279.

[11]Asahara T,Chen D,Keamey M,et al. Local delivery of vascular endothelial growth factor accelerates reendotheialization and attenuates intimal hyperplasia in balloon-injured rat carotid artery [J].Circulation,1995,91:2793-2801.

[12]Asahara T,Chen D,Keamey M,et al. Accelereted re-endothelialization and reduced neointimal thickening following catheter transfer of phVEGF165[J].J Am Coll Cardiol,1996,27(Abstract):1A.

[13]Leibovich SJ,Polverini PJ,Fong TW,et al. Production of angiogenic activity by human monocytes requires an L-arginine/nitric oxide-synthase-dependent effector mechanism [J].Proc Natl Acad Sci USA,1994,91:4190-4194.

[14]Asahsra T,Bauters C,Wu T,et al. Nitric oxide precursor augments angiogenesis and attenuates endothelial dysfunction in collateral circulation in rabbit ischemic hindlimbin vivo[J].FASEB J,1996,10(Abstract):A545.

备注/Memo

备注/Memo:
收稿日期：2001-05-24.
更新日期/Last Update: 2005-05-01