Objective:To investigate the role of vascular endothelial growth factor(VEGF)165a,VEGF165b,and VEGF receptor(VEGFR)in the development of bovine follicles.Methods:We cultured follicular cells that were collected from s...Objective:To investigate the role of vascular endothelial growth factor(VEGF)165a,VEGF165b,and VEGF receptor(VEGFR)in the development of bovine follicles.Methods:We cultured follicular cells that were collected from small,medium,and large sized bovine follicles with estrogen and measured the expression of VEGF,VEGFR2 and VEGF165b by Western blot analysis and immunofluorescence.Results:The expression of VEGF165 increased in all follicle sizes and the expression of VEGF165b was increased in the small and large follicles after culturing in an estrogen containing medium.The expression of VEGFR2 was increased in the medium and large follicles after culturing with estrogen for 96 h.VEGF165 was activated at 100 ng/mL estrogen in the large follicles for 96 h.In addition,VEGFR2 was upregulated in the medium and large follicles after treated with 100 ng/mL estrogen for 96 h.Conclusions:This evidence suggests that the expression of VEGF165 and VEGFR is associated with estrogen stimulation during the development of bovine follicles and in an autocrine or paracrine manner.This reveals an advantage during oocyte maturation in vitro.展开更多
目的研究VEGF165b和VEGF165在胃癌及癌旁正常组织中的表达及胃癌组织中VEGF165b m RNA/VEGF165 m RNA与预后的关系。方法分别应用实时RT-PCR和免疫组织化学法检测胃癌及癌旁正常组织中VEGF165b和VEGF165的基因及蛋白表达,并对患者进行2...目的研究VEGF165b和VEGF165在胃癌及癌旁正常组织中的表达及胃癌组织中VEGF165b m RNA/VEGF165 m RNA与预后的关系。方法分别应用实时RT-PCR和免疫组织化学法检测胃癌及癌旁正常组织中VEGF165b和VEGF165的基因及蛋白表达,并对患者进行2年的随访,比较VEGF165b m RNA/VEGF165 m RNA比值及这两种蛋白表达水平在胃癌及癌旁组织中的变化;同时分析VEGF165b与VEGF165蛋白表达的相关性以及胃癌组织中VEGF165b m RNA/VEGF165 m RNA与预后的关系。结果在胃癌组织中VEGF165b m RNA/VEGF165 m RNA低于癌旁正常组织中的水平;在癌旁正常组织中VEGF165b基因及蛋白表达强于VEGF165,在胃癌组织中VEGF165b基因及蛋白的表达则低于VEGF165,而且两者表达呈负相关关系;此外,在两年内死亡的患者中VEGF165b m RNA/VEGF165 m RNA明显低于生存患者中的比值水平。结论与正常组织相比,胃癌组织中存在VEGF165b向VEGF165基因及蛋白水平上的优势转换,这种变化有望成为治疗胃癌的新靶点。展开更多
目的:对比观察VEGF165b重组蛋白(recombinant human VEGF165b protein,rhVEGF165b)与贝伐珠单抗对人胃癌裸鼠移植瘤生长的影响及作用机制.方法:用人胃癌细胞BGC-823接种于裸鼠皮下,建立裸鼠移植瘤模型,随机分为3组,每组21只:rhVEGF165b...目的:对比观察VEGF165b重组蛋白(recombinant human VEGF165b protein,rhVEGF165b)与贝伐珠单抗对人胃癌裸鼠移植瘤生长的影响及作用机制.方法:用人胃癌细胞BGC-823接种于裸鼠皮下,建立裸鼠移植瘤模型,随机分为3组,每组21只:rhVEGF165b组(腹腔注射rhVEGF165b 10?g/kg)、贝伐珠单抗组(腹腔注射贝伐珠单抗5 mg/kg)、对照组(腹腔注射生理盐水10 mL/kg),分别于1、2、3 wk测量裸鼠移植瘤体积及瘤质量,免疫组织化学方法检测肿瘤组织中CD34表达(以阳性细胞数计算肿瘤微血管密度),TUNEL方法检测肿瘤组织细胞凋亡.结果:贝伐珠单抗组移植瘤体积(cm3)及瘤质量(g)在第1、2、3周均小于对照组(1 wk:0.453±0.119 vs 0.637±0.084,0.32±0.097vs 0.46±0.093;2 wk:1.691±0.381 vs 2.238±0.29,1.168±0.524 vs 2.013±0.833;3 wk:1.709±0.474 vs 4.872±0.594,1.747±0.557 vs3.463±0.986,均P<0.05),而rhVEGF165b组仅在第1、2周较对照组小(1 wk:0.546±0.132 vs0.637±0.084,1.894±0.599 vs 0.46±0.093;2wk:1.894±0.599 vs 2.238±0.29,1.537±0.568vs 2.013±0.833,均P<0.05),第3周其体积及瘤质量大于贝伐珠单抗组(3 wk:3.843±1.339 vs1.709±0.474,3.066±1.281 vs 1.747±0.557,P<0.05),与对照组无明显差异.rhVEGF165b组、贝伐珠单抗组CD34的表达水平在第1、2、3周均低于对照组(P<0.05,P<0.01),凋亡指数高于对照组(P<0.05,P<0.01);与贝伐珠单抗组相比,第1周rhVEGF165b组CD34的表达水平更低(P<0.05),但第2、3周却高于贝伐珠单抗组(P<0.01);rhVEGF165b组的凋亡指数在第1周明显高于贝伐珠单抗组(P<0.01),而第2、3周却低于贝伐珠单抗组(P<0.05).结论:rhVEGF165b、贝伐珠单抗对人胃癌移植瘤的生长有明显抑制作用,rhVEGF165b早期抑制血管生成、促进细胞凋亡表现更为明显.展开更多
目的:初步探讨VEGF165b与膀胱移行细胞癌(Transitional cell carcinoma of the bladder,TCCB)发生发展的关系。方法:用S-P免疫组化法检测38例TCCB组织和36例正常膀胱组织中VEGF165b蛋白表达;以RT-PCR法检测55例TCCB组织和43例正常膀胱...目的:初步探讨VEGF165b与膀胱移行细胞癌(Transitional cell carcinoma of the bladder,TCCB)发生发展的关系。方法:用S-P免疫组化法检测38例TCCB组织和36例正常膀胱组织中VEGF165b蛋白表达;以RT-PCR法检测55例TCCB组织和43例正常膀胱组织中VEGF165bmRNA表达。结果:正常膀胱组织中VEGF165b蛋白表达率为97.22%(35/36),TCCB组织中VEGF165b蛋白表达率为21.05%(8/38),表达差异有显著性(P<0.05);正常膀胱组织中VEGF165bmRNA阳性表达率为95.35%(41/43),明显高于TCCB组织中VEGF165bmRNA阳性表达率18.18%(10/55)(P<0.05);TCCB中VEGF165b蛋白和mRNA的表达与TCCB不同分期、分级间的表达差异具有统计学意义(P<0.05)。结论:VEGF165b在TCCB组织中的表达明显低于正常膀胱组织中的表达,这种表达差异可能与VEGF165b抑制膀胱癌的发生、发展作用有关。展开更多
Vascular endothelial growth factor 165 (VEGF165)-mediated autocrine stimulation of tumor cells enhances the progression to a malignant phenotype. VEGF165b competes with VEGF165 and binds to vascular endothelial grow...Vascular endothelial growth factor 165 (VEGF165)-mediated autocrine stimulation of tumor cells enhances the progression to a malignant phenotype. VEGF165b competes with VEGF165 and binds to vascular endothelial growth factor receptor (VEGFR), resulting in inhibition of downstream signal transduction pathways. This study was designed to investigate the role of VEGF165b in the migration and invasion of human lung adenocarcinoma A549 cells. The full-length of VEGF165b was constructed and cloned into an expression plasmid (pVEGF165b), and then transfected into A549 cells. Dimethylthiazolyl-2, 5-diphenyltetrazolium bromide (MTT) assay was used to detect the effect of VEGF165b on proliferation of transfected cells. Reverse transcription polymerase chain reaction (RT-PCR) was employed to examine the effect of VEGF165b on the expression of VEGF165 in transfected cells. Wound-healing assays were used to investigate the effect of VEGF165b on migration of transfected cells. Matrix metalloproteinase (MMPs) activity assay and in vitro invasion assay were used to determine the role of VEGF165b in invasion of transfected cells. There was no significant change in proliferation of A549 cells after transfection of pVEGF165b, but the expression of VEGF165, migration and invasion in A549 cells were inhibited. Furthermore, exogenous VEGF165b inhibited the activity of MMP9 in the supernatant of A549 cells and the subsequent invasion capacity of those cells. We therefore conclude that exogenous VEGF165b can inhibit the expression of VEGF165, as well as the migration and invasion of A549 cells, but has no effect on the proliferation of A549 cells.展开更多
文摘Objective:To investigate the role of vascular endothelial growth factor(VEGF)165a,VEGF165b,and VEGF receptor(VEGFR)in the development of bovine follicles.Methods:We cultured follicular cells that were collected from small,medium,and large sized bovine follicles with estrogen and measured the expression of VEGF,VEGFR2 and VEGF165b by Western blot analysis and immunofluorescence.Results:The expression of VEGF165 increased in all follicle sizes and the expression of VEGF165b was increased in the small and large follicles after culturing in an estrogen containing medium.The expression of VEGFR2 was increased in the medium and large follicles after culturing with estrogen for 96 h.VEGF165 was activated at 100 ng/mL estrogen in the large follicles for 96 h.In addition,VEGFR2 was upregulated in the medium and large follicles after treated with 100 ng/mL estrogen for 96 h.Conclusions:This evidence suggests that the expression of VEGF165 and VEGFR is associated with estrogen stimulation during the development of bovine follicles and in an autocrine or paracrine manner.This reveals an advantage during oocyte maturation in vitro.
文摘目的研究VEGF165b和VEGF165在胃癌及癌旁正常组织中的表达及胃癌组织中VEGF165b m RNA/VEGF165 m RNA与预后的关系。方法分别应用实时RT-PCR和免疫组织化学法检测胃癌及癌旁正常组织中VEGF165b和VEGF165的基因及蛋白表达,并对患者进行2年的随访,比较VEGF165b m RNA/VEGF165 m RNA比值及这两种蛋白表达水平在胃癌及癌旁组织中的变化;同时分析VEGF165b与VEGF165蛋白表达的相关性以及胃癌组织中VEGF165b m RNA/VEGF165 m RNA与预后的关系。结果在胃癌组织中VEGF165b m RNA/VEGF165 m RNA低于癌旁正常组织中的水平;在癌旁正常组织中VEGF165b基因及蛋白表达强于VEGF165,在胃癌组织中VEGF165b基因及蛋白的表达则低于VEGF165,而且两者表达呈负相关关系;此外,在两年内死亡的患者中VEGF165b m RNA/VEGF165 m RNA明显低于生存患者中的比值水平。结论与正常组织相比,胃癌组织中存在VEGF165b向VEGF165基因及蛋白水平上的优势转换,这种变化有望成为治疗胃癌的新靶点。
文摘目的:对比观察VEGF165b重组蛋白(recombinant human VEGF165b protein,rhVEGF165b)与贝伐珠单抗对人胃癌裸鼠移植瘤生长的影响及作用机制.方法:用人胃癌细胞BGC-823接种于裸鼠皮下,建立裸鼠移植瘤模型,随机分为3组,每组21只:rhVEGF165b组(腹腔注射rhVEGF165b 10?g/kg)、贝伐珠单抗组(腹腔注射贝伐珠单抗5 mg/kg)、对照组(腹腔注射生理盐水10 mL/kg),分别于1、2、3 wk测量裸鼠移植瘤体积及瘤质量,免疫组织化学方法检测肿瘤组织中CD34表达(以阳性细胞数计算肿瘤微血管密度),TUNEL方法检测肿瘤组织细胞凋亡.结果:贝伐珠单抗组移植瘤体积(cm3)及瘤质量(g)在第1、2、3周均小于对照组(1 wk:0.453±0.119 vs 0.637±0.084,0.32±0.097vs 0.46±0.093;2 wk:1.691±0.381 vs 2.238±0.29,1.168±0.524 vs 2.013±0.833;3 wk:1.709±0.474 vs 4.872±0.594,1.747±0.557 vs3.463±0.986,均P<0.05),而rhVEGF165b组仅在第1、2周较对照组小(1 wk:0.546±0.132 vs0.637±0.084,1.894±0.599 vs 0.46±0.093;2wk:1.894±0.599 vs 2.238±0.29,1.537±0.568vs 2.013±0.833,均P<0.05),第3周其体积及瘤质量大于贝伐珠单抗组(3 wk:3.843±1.339 vs1.709±0.474,3.066±1.281 vs 1.747±0.557,P<0.05),与对照组无明显差异.rhVEGF165b组、贝伐珠单抗组CD34的表达水平在第1、2、3周均低于对照组(P<0.05,P<0.01),凋亡指数高于对照组(P<0.05,P<0.01);与贝伐珠单抗组相比,第1周rhVEGF165b组CD34的表达水平更低(P<0.05),但第2、3周却高于贝伐珠单抗组(P<0.01);rhVEGF165b组的凋亡指数在第1周明显高于贝伐珠单抗组(P<0.01),而第2、3周却低于贝伐珠单抗组(P<0.05).结论:rhVEGF165b、贝伐珠单抗对人胃癌移植瘤的生长有明显抑制作用,rhVEGF165b早期抑制血管生成、促进细胞凋亡表现更为明显.
文摘目的:初步探讨VEGF165b与膀胱移行细胞癌(Transitional cell carcinoma of the bladder,TCCB)发生发展的关系。方法:用S-P免疫组化法检测38例TCCB组织和36例正常膀胱组织中VEGF165b蛋白表达;以RT-PCR法检测55例TCCB组织和43例正常膀胱组织中VEGF165bmRNA表达。结果:正常膀胱组织中VEGF165b蛋白表达率为97.22%(35/36),TCCB组织中VEGF165b蛋白表达率为21.05%(8/38),表达差异有显著性(P<0.05);正常膀胱组织中VEGF165bmRNA阳性表达率为95.35%(41/43),明显高于TCCB组织中VEGF165bmRNA阳性表达率18.18%(10/55)(P<0.05);TCCB中VEGF165b蛋白和mRNA的表达与TCCB不同分期、分级间的表达差异具有统计学意义(P<0.05)。结论:VEGF165b在TCCB组织中的表达明显低于正常膀胱组织中的表达,这种表达差异可能与VEGF165b抑制膀胱癌的发生、发展作用有关。
基金supported by grant from the National Natural Sciences Foundation of China (No. 30973473)
文摘Vascular endothelial growth factor 165 (VEGF165)-mediated autocrine stimulation of tumor cells enhances the progression to a malignant phenotype. VEGF165b competes with VEGF165 and binds to vascular endothelial growth factor receptor (VEGFR), resulting in inhibition of downstream signal transduction pathways. This study was designed to investigate the role of VEGF165b in the migration and invasion of human lung adenocarcinoma A549 cells. The full-length of VEGF165b was constructed and cloned into an expression plasmid (pVEGF165b), and then transfected into A549 cells. Dimethylthiazolyl-2, 5-diphenyltetrazolium bromide (MTT) assay was used to detect the effect of VEGF165b on proliferation of transfected cells. Reverse transcription polymerase chain reaction (RT-PCR) was employed to examine the effect of VEGF165b on the expression of VEGF165 in transfected cells. Wound-healing assays were used to investigate the effect of VEGF165b on migration of transfected cells. Matrix metalloproteinase (MMPs) activity assay and in vitro invasion assay were used to determine the role of VEGF165b in invasion of transfected cells. There was no significant change in proliferation of A549 cells after transfection of pVEGF165b, but the expression of VEGF165, migration and invasion in A549 cells were inhibited. Furthermore, exogenous VEGF165b inhibited the activity of MMP9 in the supernatant of A549 cells and the subsequent invasion capacity of those cells. We therefore conclude that exogenous VEGF165b can inhibit the expression of VEGF165, as well as the migration and invasion of A549 cells, but has no effect on the proliferation of A549 cells.