血管内皮生长因子D和血管内皮生长因子E

血管内皮生长因子是一种分泌型糖蛋白 ,是调节血管生成最重要的细胞因子。近年又发现了几种新的与之结构和功能类似的因子 ,它们组成了血管内皮生长因子家族 ,通过与其受体组成的复杂的网络信号传导系统 ,调节生物体内脉管系统的发生和发展 ,参与多种生理病理过程。     

血管内皮生长因子的研究进展

血管内皮生长因子 (Vascular endothelial growth fac-tor,VEGF)又叫血管通透性因子 (Vascular permeabilityfactor,VPF)或血管调理素 (Vasculotropin)。是 1989年从牛垂体滤泡星状细胞培养液中纯化出来的蛋白质〔1〕,能高度特异地作用于血管内皮细胞的有丝分裂原。本文就 VEGF的分子结构特征、生物学特性以及临床治疗方面作一简要介绍。1　 VEGF的分子结构特征及组织器官分布VEGF是由两个相同多肽链通过二硫键交联形成的同型二聚体糖蛋白化合物 〔2〕,分子量在 34～ 45 KD之间 ,具有高度的保守性 ,对热和酸稳定 ,与乙酰肝素蛋白…     

血管内皮生长因子家族

血管内皮生长因子是重要的血管生成因子 ,在生理及病理性血管生成中有十分重要的作用。近年发现其不是单一因子 ,还有其它因子与之相关 ,称为血管内皮生长因子家族。     

血管内皮生长因子研究进展

血管内皮生长因子(VEGF)是一种能特异地作用于血管内皮细胞的生长因子。在生理和病理情况下均有表达。本文就VEGF的分子特征、VEGF受体及信号传导机制、表达调节和生物学特征作一综述。     

血管内皮生长因子与血管生成

本文综述了血管内皮生长因子结构特点、体内分布、正常及病理条件下的表达水平变化及其生物学功能、并对血管通透性与血管生成之间的关系进行了评述.     

血管内皮生长因子

血管内皮生长因子（ＶＥＧＦ）具有促进内皮细胞增殖，提高血管通透性，改变细胞外基质等生物学作用，在血管的发生中发挥重要作用。ＶＥＧＦ与类风湿性关节炎、糖尿病性视网膜病等多种疾病的发生密切相关。肿瘤组织可合成和分泌ＶＥＧＦ，ＶＥＧＦ在肿瘤组织中的表达水平比周围的正常组织高，并与肿瘤的恶性程度相关。     

血管内皮生长因子与肿瘤

血管内皮生长因子（Ｖａｓｃｕｌａｒｅｎｄｏｔｈｅｌｉａｌｇｒｏｗｔｈｆａｃｔｏｒ，ＶＥＧＦ）是目前研究的热点 ,因为它参与了许多生理和病理过程的血管生成 ,包括胚胎发育 ,创伤修复 ,肿瘤生长 ,心肌缺血 ,视网膜血管病变以及类风湿性关节炎这样的慢性炎症疾病 ［１］。     

血管内皮生长因子受体2的结构功能与信号转导

Angiogenesis, or the formation of new blood vessels out of pre - existing capillaries, is very important in many physiologic and pathologic processes, such as embryonic development, cancer, retinopathies, etc. Vascular endothelial growth factor receptor - 2 (VEGFR-2) plays a key role in angiogenesis. In this review, we discussed the structure, function and signal transduction of vascular endothelial growth factor receptor-2. Understanding these should provide important insights into how new strategies can be devised to interfere in the physiologic and pathologic processes involved in angiogensis.     

血管内皮生长因子与妇科肿瘤

血管内皮生长因子(VEGF)是特异性作用于血管内皮细胞,并促进其有丝分裂的一类活性物质,在多种肿瘤组织中均有表达.妇科肿瘤组织存在VEGF及其受体的高表达,VEGF可能与妇科肿瘤的发生、发展及预后有关.采用现代分子生物学方法阻止VEGF及其受体表达,可抑制肿瘤生长.     

血管内皮生长因子与心肌缺血

血管内皮生长因子是一种特异作用于血管内皮细胞的多功能细胞因子，有很强的促血管形成作用，能刺激血管内皮细胞分裂和迁移。在胚胎发育、肿瘤和心血管等疾病的发病和防治中具有重要作用，尤其在血管病变和与血管生成有关疾病的研究中有重要意义。它有可能成为预防心肌缺血、治疗心肌梗塞的另一条很有希望的途径。     

血管内皮细胞生长因子对内皮细胞凋亡拮抗作用的研究

目的 :初步探讨缺氧对培养人脐静脉内皮细胞凋亡的影响及血管内皮生长因子的干预性影响。方法 :( 1)人脐静脉内皮细胞的培养及鉴定。 ( 2 )建立人脐静脉内皮细胞缺氧模型 ,TUNEL法观测不同缺氧时间 ( 0、12、2 4、48h)对内皮细胞凋亡的影响及不同剂量血管内皮生长因子的拮抗作用。结果 :随缺氧时间延长 ,HUVECs凋亡率显著升高 ,呈时间相关性 ;血管内皮生长因子显著抑制缺氧导致的内皮细胞凋亡 ,呈剂量相关性。结论 :缺氧作为一种致病因素 ,对内皮细胞凋亡的促发作用是随缺氧时间的延长而加重的。内皮细胞的过度凋亡是引起内皮功能障碍的一个重要因素 ,血管内皮生长因子通过抑制内皮细胞凋亡 ,而具有内皮细胞保护作用。     

Human Herpesvirus-8-Transformed Endothelial Cells Have Functionally Activated Vascular Endothelial Growth Factor/Vascular Endothelial Growth Factor Receptor

Kaposi's sarcoma is a vascular tumor commonly associated with human immunodeficiency virus (HIV)-1 and human herpesvirus (HHV-8) also known as Kaposi's sarcoma-associated herpesvirus. The principal features of this tumor are abnormal proliferation of vascular structures lined with spindle-shaped endothelial cells. HHV-8 may transform a subpopulation of endothelial cells in vitro via viral and cellular gene expression. We hypothesized that among the cellular genes, vascular endothelial growth factors (VEGFs) and their cognate receptors may be involved in viral-mediated transformation. We have shown that HHV-8-transformed endothelial cells (EC-HHV-8) express higher levels of VEGF, VEGF-C, VEGF-D, and PlGF in addition to VEGF receptors-1, -2, and -3. Furthermore, antibodies to VEGF receptor-2 inhibited cell proliferation and viability. Similarly, inhibition of VEGF gene expression with antisense oligonucleotides inhibited EC-HHV-8 cell proliferation/viability. The growth and viability of primary endothelial cells and a fibroblast cell line however were unaffected by either the VEGF receptor-2 antibody or the VEGF antisense oligodeoxynucleotides. VEGF and VEGF receptors are thus induced in EC-HHV-8 and participate in the transformation. Inhibitors of VEGF may thus modulate the disease process during development and progression.     

人脑胶质瘤VEGF的表达和微血管检测及意义

目的探讨人脑胶质瘤中血管内皮细胞生长因子(VEGF)的表达与微血管数量(MVQ)和肿瘤良恶性程度的关系. 方法用免疫组织化学染色方法检测手术切除石蜡包埋的47例人脑胶质瘤(Ⅰ～Ⅱ级22例,Ⅲ级15例,Ⅳ级10 例)组织中的VEGF蛋白表达情况和MVQ数量,借助显微镜观察其阳性细胞数和阳性血管数; 另外,分别取脑外伤后开颅内减压术中切除的正常脑组织10例作为对照组. 结果①正常脑组织未检测到VEGF蛋白的表达,而MVQ数量少 ,表达强度弱;②各级别胶质瘤组织中均有VEGF和MVQ表达,主要表达于肿瘤细胞的胞浆和血管内皮细胞胞膜中;③3组胶质细胞瘤中VEGF的表达阳性率分别为22.2%、86.7%、90%、Ⅰ～Ⅱ级组与其它两组间差异有显著性意义(p<0.05;p<0.01),VEGF表达阳性组的MVQ平均值(46.8±12.4)明显高于阴性组MVQ值 (22.4±11.5)(p<0.01);④VEGF的表达与MVQ相关(r=0.75, p <0.001). 结论①VEGF在脑胶质瘤血管生成中起重要作用 ,能促进胶质瘤血管的形成;②VEGF和MVQ与胶质瘤良恶性程度明显相关,可作为脑胶质瘤病理诊断的补充指标;③VEGF可作为治疗脑胶质瘤的靶向,为胶质瘤的基因治疗提供指导方向.     

Immunohistochemical Expression of Vascular Endothelial Growth Factor in Canine Mammary Tumours

The histopathological and clinical aspects of canine mammary tumours (CMTs) have been widely studied, but the variation in the biological behaviour of these neoplasms hampers the identification of prognostic factors. Sustained angiogenesis has been suggested to be one of the most important factors underlying tumour growth and invasion. This process involves the action of several growth factors including vascular endothelial growth factor (VEGF). The present study characterizes the relationship between immunohistochemical expression of VEGF and gross (e.g. size and tissue fixation) and microscopical (e.g. type, growth, necrosis, lymphoid infiltration, lymph node metastasis, histological grade and proliferation index) features of CMTs. Forty-eight benign and 64 malignant CMTs were evaluated. Statistical analysis failed to show a significant relationship between VEGF expression and the pathological features, suggesting that VEGF expression occurs in both benign and malignant tumours and is independent of histological type, proliferation, tissue invasion or local metastatic capacity.     

VEGF在翼状胬肉发病与复发中的作用

目的：探讨血管内皮生长因子（VEGF）在翼状胬肉发病与复发中的作用。方法：采用免疫组织化学方法检测42例初发与30例复发翼状胬肉标本中VEGF的表达情况,并与30例正常对照组比较。结果：VEGF表达阳性率：对照组为6.7%（2/30）,初发组为61.9%（26/42）,复发组为93.3%（28/30）,对照组低于初发组（P〈0.01）,初发组低于复发组（P〈0.05）。VEGF表达强阳性率：对照组为0%（0/30）,初发组为26.2%（11/42）,复发组为63.3%（19/30）,对照组低于初发组（P〈0.01）,初发组低于复发组（P〈0.01）。结论：VEGF的高水平表达是翼状胬肉发病与复发的重要原因。     

血管内皮生长因子与甲状腺疾病研究进展

血管内皮生长因子(VEGF)的基本功能是促进血管生长。近年研究表明,VEGF通过影响病灶处血管或癌细胞自身的生成从而在多种甲状腺疾病中发挥着重要作用。但VEGF的功能以及在不同甲状腺疾病中的具体变化情况仍然需要进一步探索。本文对VEGF的分子生物学及生物学特性、在多种甲状腺疾病中的作用及其临床应用进行简要综述。     

Vascular Endothelial Growth Factor (VEGF) in Autoimmune Diseases

Vascular endothelial growth factor (VEGF) is a potent stimulating factor for angiogenesis and vascular permeability. There are eight isoforms with different and sometimes overlapping functions. The mechanisms of action are under investigation with emerging insights into overlapping pathways and cross-talk between other receptors such as the neuropilins, which were not previously associated to angiogenesis. VEGF has important physiological actions on embryonic development, healing, and menstrual cycle. It also has a great role in pathological conditions that are associated to autoimmune diseases. There is considerable evidence in various autoimmune diseases such as in systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis of an interrelationship between the VEGF system and theses disorders. Serum levels of VEGF correlate with disease activity in a large number of autoimmune diseases and fall with the use of standard therapy. We raised the possible future therapeutic strategies in autoimmune diseases with the anti-VEGF or anti-VEGFR (receptor). So far, this therapy has been used in cancer and macular ocular degeneration in diabetes. This review outlines the evidence for VEGF participation in various autoimmune diseases and proposes lines for future research in this field.     

Expression of Vascular Endothelial Growth Factor Isoforms in the Japanese Quail Embryo

Vascular endothelial growth factor (VEGF) is required for vascular development. In the quail, four VEGF isoforms formed by alternative splicing, are translated into proteins with 122, 146, 166, and 190 amino acids. VEGF isoforms differ biochemically, with variable affinities for heparan sulfate proteoglycans, the extracellular matrix and VEGF receptors. There are few data on the functional significance of VEGF isoforms. RT-PCR was used to examine isoform expression during quail vascular development. Our results suggest that all quail isoforms are expressed during establishment of the vascular pattern in whole embryos and extraembryonic tissues at apparently equal levels. No isoform-specific expression patterns were detected in isolated endoderm or between embryo halves.     

The Secretion of Endothelin-1 by Microvascular Endothelial Cells from Human Benign Prostatic Hyperplasia is Inhibited by Vascular Endothelial Growth Factor

Prostate growth seems to be influenced by paracrine factors like endothelin-1 (ET-1), originating from the microvascular endothelium. Recently, we reported on the first isolation and primary culture of microvascular endothelial cells (HPEC) derived from tissue of human benign prostatic hyperplasia (BPH). Therefore, direct investigation of growth factor secretion by HPEC is now possible.

BPH tissue was cut into small cubes and gently squeezed after incubation with dispase. HPEC were cultured from the resulting cell suspension after a stepwise selection by use of superparamagnetic beads coated with antibodies against endothelial specific antigens. HPEC were characterized by flow cytometry. After the incubation of HPEC either with vascular endothelial growth factor (VEGF), tumor necrosis factor α (TNF-α), or adenosine triphosphate (ATP), the secretion of ET-1 was measured by ELISA.

HPEC showed a typical endothelial morphology. They were positive for von Willebrand factor and CD31. The ET-1 secretion of HPEC was inhibited by VEGF, but was unaffected by TNF-α or ATP. Furthermore, histochemistry revealed that in vivo microvascular endothelial cells were negative for ET-1. Because of the suppression by the widespread VEGF, it is unlikely that ET-1 from the microvascular endothelium acts as a growth factor in human BPH.