内皮细胞脂质过氧化损伤与平滑肌细胞增殖的关系
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The Relationship Between Lipid Peroxidation Injury to Endothelial Cells and the Proliferation of Smooth Muscle Cells
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    摘要:

    用联胺(diamide)作用于培养的人脐静脉内皮细胞引起其脂质过氧化损伤;用抗碱性纤维母细胞生长因子(basicfibroblastgrowthfactor,bFGF)单克隆抗体和抗血小板源性生长因子BB(plateletderivedgrowthfactorBB,PDGF-BB)多克隆抗体进行免疫组织化学染色,以检测内皮细胞暴露于联胺前后bFGF和PDF-BB的表达;以及其条件培养基对平滑肌细胞(smoothmusclecells,SMC)内bFGF表达的影响。用H3-TdR掺入法观察内皮细胞暴露于联胺后其条件培养基对SMC是否有增殖活性。结果显示,联胺引起内皮细胞脂质过氧化损伤后,其PDGF-BB和bFGF表达增多,同时其条件培养基促进SMC表达bFGF,并对SMC有明显的促有丝分裂作用;提示,内皮细胞的脂质过氧化损伤可诱导其产生生长因子,刺激SMC增殖,在动脉粥样硬化斑块形成中起一定的作用。

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    Aim To understand the interaction of endothelial cells(EC)with arterial smooth muscle cells (SMC),the relationship between lipid peroxidation injury to cultured human umbilical vein EC and the proliferation of cultured arterial SMC was investigated.Methods The lipid peroxidation injury to cultured EC was induced by the treatment of diamide,and the content of terminal metabolite of cellular lipid peroxides malonaldehyde was determined by the method described by Hisayuki.The expression of both basic fibroblast growth factor(bFGF)and platelet derived growth factor BB(PDGF-BB)in EC after exposed to diamide was examined by immunohistochemistry using a mouse anti-human bFGF monoclonal antibody and a mouse anti-human PDGF-BB polyoclonal antibody,respectively,and the expression of bFGF in SMC after exposed to the medium conditioned by diamide stimulated EC(dsEC-CM )was examined by the same method as well.The incorporation of H thymidine into DNA in the cells was used to observe the mito genic effect of dsEC-CM on SMC.Results Diamide induces lipid peroxidation injury to cultured EC resulting in the increased expression of bFGF and PIX.F-BB in the cells.dsEC-CM could in duce the expression of bFGF in SMC, and was obviously proliferation for SMC.Conclusions The lipid peroxidation injury to EC may play a role in atherogenesis through inducing the production of some growth factors that stimulate the proliferation of SMC.

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夏春枝,邓仲端,李丽珠,瞿智玲.内皮细胞脂质过氧化损伤与平滑肌细胞增殖的关系[J].中国动脉硬化杂志,1996,4(3):181.

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