中华病理学杂志
中華病理學雜誌
중화병이학잡지
Chinese Journal of Pathology
2015年
4期
270-273
,共4页
血管生成蛋白质类%内皮生长因子%细胞迁移分析%细胞外信号调节MAP激酶类
血管生成蛋白質類%內皮生長因子%細胞遷移分析%細胞外信號調節MAP激酶類
혈관생성단백질류%내피생장인자%세포천이분석%세포외신호조절MAP격매류
Angiogenic proteins%Endothelial growth factors%Cell migration assays%Extracellular signal-regulated MAP kinases
目的:探讨类表皮生长因子域7(EGFL7)对内皮细胞迁移和血管生成的影响。方法以人微血管内皮细胞为研究对象,构建EGFL7过表达载体,转染入细胞。应用即时定量PCR法检测EGFL7 mRNA表达水平及Western blot检测EGFL7蛋白表达水平。分别采用划痕实验法、Matrigel法观察EGFL7对内皮细胞迁移及血管生成的影响。 Western blot检测内皮细胞转染EGFL7过表达载体和空载体0、10、30和60 min后,p-AKT、AKT、p-ERK和ERK蛋白表达情况。结果 EGFL7过表达组可以显著促进内皮细胞的迁移、血管生成;EGFL7可以激活ERK信号通路,但对AKT信号通路几乎无影响;抑制 ERK 信号通路后, EGFL7对内皮细胞迁移和血管生成的影响均显著下降。结论EGFL7通过ERK信号通路影响内皮细胞迁移和血管生成。
目的:探討類錶皮生長因子域7(EGFL7)對內皮細胞遷移和血管生成的影響。方法以人微血管內皮細胞為研究對象,構建EGFL7過錶達載體,轉染入細胞。應用即時定量PCR法檢測EGFL7 mRNA錶達水平及Western blot檢測EGFL7蛋白錶達水平。分彆採用劃痕實驗法、Matrigel法觀察EGFL7對內皮細胞遷移及血管生成的影響。 Western blot檢測內皮細胞轉染EGFL7過錶達載體和空載體0、10、30和60 min後,p-AKT、AKT、p-ERK和ERK蛋白錶達情況。結果 EGFL7過錶達組可以顯著促進內皮細胞的遷移、血管生成;EGFL7可以激活ERK信號通路,但對AKT信號通路幾乎無影響;抑製 ERK 信號通路後, EGFL7對內皮細胞遷移和血管生成的影響均顯著下降。結論EGFL7通過ERK信號通路影響內皮細胞遷移和血管生成。
목적:탐토류표피생장인자역7(EGFL7)대내피세포천이화혈관생성적영향。방법이인미혈관내피세포위연구대상,구건EGFL7과표체재체,전염입세포。응용즉시정량PCR법검측EGFL7 mRNA표체수평급Western blot검측EGFL7단백표체수평。분별채용화흔실험법、Matrigel법관찰EGFL7대내피세포천이급혈관생성적영향。 Western blot검측내피세포전염EGFL7과표체재체화공재체0、10、30화60 min후,p-AKT、AKT、p-ERK화ERK단백표체정황。결과 EGFL7과표체조가이현저촉진내피세포적천이、혈관생성;EGFL7가이격활ERK신호통로,단대AKT신호통로궤호무영향;억제 ERK 신호통로후, EGFL7대내피세포천이화혈관생성적영향균현저하강。결론EGFL7통과ERK신호통로영향내피세포천이화혈관생성。
Objective To explore the effect of epidermal growth factor-like domain 7 ( EGFL7 ) on the migration and angiogenesis of endothelial cells.Methods EGFL7 overexpression vectors were constructed and transfected into human microvascular endothelial cells.The expression levels of EGFL7-mRNA and EGFL7 protein were examined by real-time RT-PCR and Western blot.Cell migration was analyzed by the wound healing.The capability of cell to form capillary-like tubes in vitro was evaluated on matrigel assay.Protein expression of p-AKT, AKT, p-ERK and ERK in endothelial cells was detected by Western blot upon transfection with EGFL7 overexpression vectors and vehicle control for 0, 10, 30 and 60 min. Results Migration and angiogenesis of endothelial cells were notably enhanced by EGFL7 overexpression.ERK pathway was strongly activated by EGFL7, whereas AKT remained constant in endothelial cells.Inhibition of ERK impaired EGFL7 induced ERK activation and endothelial cell migration and angiogenesis. Conclusion EGFL7 effectively promotes migration and angiogenesis through ERK signaling pathway in endothelial cells.