神经生长因子在血管生成中的研究进展

神经生长因子（NGF）是近年来治疗性血管生成研究领域的热点.NGF在神经的生长、发育、分化、存活等方面发挥着不可或缺的作用,同时NGF还可以促进内皮细胞、血管平滑肌细胞等的迁移、分化,甚至动员外周内皮祖细胞促进其活化,进而促进新生血管的形成。也可在与血管内皮生长因子的互相作用下促进内皮细胞的增生、迁移、分化,从而完成血管生成的过程.其在神经与血管的发生、发展中的重要作用为治疗外周动脉缺血性疾病打开了新的思路。     

促血管生成素在机体血管形成过程中的作用

促血管生成素 (angiopoietins,Ang)及其受体Tie2系统是调控血管完整性的重要因子 ,并参于生理及病理性血管生成 ,Ang1促进血管成熟与稳定 ,并维持血管的完整性。在内源性血管内皮细胞生长因子 (vascularendothelialgrowthfactor ,VEGF)作用存在时 ,Ang2可增加毛细管管径、重建基膜、促EC增生与迁移 ,刺激新生血管出芽 ,而当内源性VEGF作用受抑制时Ang2加速内皮细胞死亡及血管退行性变。推测使用Ang、VEGF联合用于治疗性血管生成可能使新生血管获得持久稳定的结构 ,达到更理想的远期疗效。     

促血管生成素在机体血管形成过程中的作用

促血管生成素(angiopoietins，Ang)及其受体Tie2系统是调控血管完整性的重要因子，并参于生理及病理性血管生成，Ang1促进血管成熟与稳定，并维持血管的完整性。在内源性血管内皮细胞生长因子(vascular endothelial growth factor，VEGF)作用存在时，Ang2可增加毛细管管径、重建基膜、促EC增生与迁移，刺激新生血管出芽，而当内源性VEGF作用受抑制时Ang2加速内皮细胞死亡及血管退行性变。推测使用Ang、VEGF联合用于治疗性血管生成可能使新生血管获得持久稳定的结构，达到更理想的远期疗效。     

血管内皮生长因子与肿瘤血管生成

目的 评价血管内皮生长因子（VEGF）对肿瘤血管生成的影响及其在肿瘤治疗中的应用。方法 通过对近年来血管内皮生长因子促进肿瘤血管生成方面的相关文献回顾,总结VEGF研究的进展,介绍抗血管生成治疗在肿瘤生物治疗中的作用。结果 血管生成在肿瘤生长中的重要地位已经被证实。在众多的促进肿瘤血管生成因素中,VEGF起到最基础和最关键的作用。针对VEGF的抗肿瘤血管生成的治疗已取得了很大进展,包括应用VEGF抑制剂、腺病毒介导的基因治疗等。结论 VEGF是主要的促进肿瘤血管生成的物质,针对VEGF的抗血管生成治疗可能给恶性肿瘤的治疗带来新的契机。     

血管内皮生长因子防治骨质疏松的研究进展

血管内皮生长因子(vascular endothelial growth factor,VEGF)与骨质疏松的发生关系密切。其不仅能够促进血管生成,亦在骨形成与重建过程中发挥着重要的作用。现代研究表明,其能够促进内皮细胞增殖及新血管生成,加速骨形成及重建过程,直接促进骨髓间充质干细胞及增加成骨细胞的成骨活性,降低破骨细胞溶骨活性来促进骨形成及增加骨密度,在骨质疏松的发生发展中起到重要的作用。本文就VEGF对骨形成过程中相关细胞的作用及其机制做一分析总结,综述近年来研究进展及临床治疗效果,旨在为今后相关研究及骨质疏松临床治疗提供指导。     

血管内皮生长因子在甲状腺癌的表达及意义

血管内皮生长因子特异性作用于血管内皮细胞,通过促进内皮细胞的增生,增加血管通透性,以诱导肿瘤血管及淋巴管生成,在肿瘤的发生发展中起到关键作用.研究表明,VEGF及其受体的表达与甲状腺癌的发生,淋巴结转移,预后密切相关,抑制VEGF及其受体的表达在甲状腺未分化癌及髓样癌的治疗中有一定的应用前景.     

血管内皮生长因子与男性生殖系统的血管生成

血管内皮生长因子 (VEGF)是最重要的血管生成促进因子 ,其主要功能有诱导血管通透性增加 ,促进血管内皮细胞迁移 ,刺激内皮细胞增殖进而促进血管生成。本文就VEGF在男性前列腺、睾丸、附睾的定位、表达调控 ,以及其变化所导致的血管生成的改变与男性生殖系统某些疾病的关系作一简要综述     

VEGF在神经外科疾病中的作用

许多生理过程和病理过程都依赖于血管生成,调控血管生成因子很多,其中以血管内皮细胞生长因子尤为重要.血管内皮生长因子(vascular endothelialgrowth factor,VEGF)又称血管通透因子(vascular permeabilitv factor,VPF),主要作用于血管内皮细胞,促进内皮细胞存活和增殖,还有增加血管通透性的作用.本文主要探讨VEGF在神经外科疾病中所起的作用.     

血管生成素/Tie2信息通路在血管形成中的调节作用(文献综述)

血管生成素(Angiopoietins,AP)/Tie2是一种新发现的调节血管生成的重要信息途径.AP-1促进内皮细胞受体Tie2磷酸化,吸引血管平滑肌细胞、周细胞等血管周围细胞包围、支持内皮细胞,促进血管重塑、成熟,并维持血管的完整性和调节血管功能;AP-2竞争抑制AP-1的作用,在VEGF等促血管形成因子存在时促进血管生成;当缺乏血管形成因子时,AP-2则参与新生血管的消退过程.     

慢病毒介导的血管内皮生长因子干扰对瘢痕成纤维细胞及内皮细胞的影响

增生性瘢痕是创面愈合过程中的病理现象,严重影响患者的容貌、外观,有的甚至引发功能障碍.在临床上,瘢痕进展的过程中皮肤颜色的变化提示瘢痕的形成和成熟与组织中血管的作用有关.抗血管生成可能能够治疗增生性瘢痕.本实验室前期已构建了针对人血管内皮生长因子(VEGF)的干扰慢病毒,本研究拟在体外瘢痕成纤维细胞培养模型上探讨稳定的干扰VEGF对成纤维细胞的影响和内皮细胞的影响.     

Effects of androgen suppression and radiation on prostate cancer suggest a role for angiogenesis blockade

Antiandrogen therapy is an important modality in the treatment of prostate cancer. Recent research into the role of angiogenesis in tumour growth and metastasis has uncovered links between antiandrogen therapy, radiation therapy and angiogenesis, which have exciting implications for the treatment of prostate cancer. Angiogenic cytokines such as vascular endothelial growth factor (VEGF) have been identified in prostate cancer cells and tumours, and androgens appear to stimulate VEGF. This article assesses the antiangiogenic effects of hormonal therapy and assesses the role that angiogenesis may play in the observed cooperation between hormonal and radiation therapies for prostate cancer.     

慢性颅内静脉压增高状态下硬脑膜血管内皮生长因子的表达与超微结构变化

目的探讨慢性颅内静脉压增高状态下硬脑膜血管内皮生长因子(VEGF)表达及其与血管超微结构改变的关系。方法选Wistar雄性大鼠24只(实验组12只;对照组12只),右侧颈总动脉和颈外静脉端端吻合,同时结扎上矢状窦,建立慢性颅内静脉压增高的动物模型;90d后采用免疫组织化学方法检测硬脑膜血管内皮细胞中VEGF的表达和血管生成情况,透射电镜观察血管壁超微结构变化。结果B组的硬脑膜血管中VEGF仅呈微弱表达,其吸光度值(A)为2.12±0.59,A组硬脑膜中血管内皮细胞VEGF表达吸光度值(A)为8.66±1.75,两者相比A组微血管生成数量显著增高(P<0.05);微血管密度(×200倍计数)B组为(2.25±0.23/0.74)mm2,A组为(8.66±1.75/0.74)mm2,两者相比A组微血管生成密度显著增高(P<0.05)。而且A组血管内皮细胞的间隙增宽,平滑肌数量减少,胶原组织增多。结论慢性静脉压增高状态下硬脑膜血管中VEGF表达升高,可能与血管生成及血管的超微结构改变有重要关系     

VEGF、KDR的表达对肝癌的血管生成、生长、转移的影响

目的　研究血管内皮生长因子 (VEGF)及其受体KDR(kinaseinsertdomaincontainingre ceptor)对肝细胞肝癌的血管生成、生长、转移等方面的影响。　方法　对 45例肝癌、2 1例肝硬化、8例正常肝标本进行了免疫组化、原位杂交染色 ,然后行图像分析 ,观察VEGF、KDR的表达与肝癌病理特点之间的关系 ,并进行统计学分析。　结果　肝细胞肝癌中VEGF高表达 ;并与肝癌的血管生成相关 ;VEGF的表达强度与表达率均与肝癌的转移、包膜形成相关 ;KDR不仅表达于血管内皮细胞 ,还表达于部分肝癌细胞。　结论　VEGF在肝癌的血管生成、癌细胞转移、包膜形成中可能起到重要作用 ,KDR在肝癌细胞的表达可能是一种自分泌行为。     

血管内皮生长因子:从血管形成到神经元保护

血管内皮生长因子(vascular endotjelial growthfactor,VEGF)是一类多功能的生长因子。它具有促进内皮细胞增殖、诱导血管形成的作用,因而被应用于缺血性血管疾病(如缺血性心肌病和下肢缺血)的治疗,并成为近年来心血管病研究的热点之一。新近研究发现,VEGF及其受体在中枢神经组     

Loss of the VEGF(164) and VEGF(188) isoforms impairs postnatal glomerular angiogenesis and renal arteriogenesis in mice

Vascular endothelial growth factor (VEGF) is transcribed in the VEGF(120), VEGF(164), or VEGF(188) isoforms, which differ in receptor binding, matrix association, and angiogenic activity. This vascular growth factor has been implicated in the development of the renal vasculature, but the role of the distinct VEGF isoforms remains unknown. In the present report, renal angiogenesis and arteriogenesis were studied in VEGF(120/120) mice, expressing only the short VEGF(120) isoform. In VEGF(120/120) mice, ingrowth and survival of capillaries in glomeruli, remodeling of peritubular capillaries, vascular coverage by pericytes, and branching of renal arteries were all severely impaired, causing abnormal glomerular filtration and impairing renal function. The arterial branching defect might be related to a reduced expression of renin, a presumed renal arterial branching factor. Glomerulosclerosis and tubular dilation possibly resulted from renal ischemia caused by vascular defects. Thus, VEGF(164) and VEGF(188) not only mediate angiogenesis, but they also play an essential role in renal branching arteriogenesis.     

Normoxic wound fluid contains high levels of vascular endothelial growth factor.

OBJECTIVE: To examine the temporal integration of vascular endothelial growth factor (VEGF), which has been shown to be present in wound fluid, with the putatively related processes of wound fluid oxygen content, wound angiogenesis, and granulation tissue formation. SUMMARY BACKGROUND DATA: During cutaneous wound repair, new tissue formation starts with reepithelialization and is followed by granulation tissue formation, including neutrophil and macrophage accumulation, fibroblast ingrowth, matrix deposition, and angiogenesis. Because angiogenesis and increased vascular permeability are characteristic features of wound healing, VEGF may play an important role in tissue repair. METHODS: A ventral hernia, surgically created in the abdominal wall of female swine, was repaired using silicone sheeting and skin closure. Over time, a fluid-filled wound compartment formed, bounded by subcutaneous tissue and omentum. Ultrasonography was performed serially to examine the anatomy and dimensions of the subcutaneous tissue and wound compartment. Serial wound fluid samples, obtained by percutaneous aspiration, were analyzed for PO2, PCO2, pH, and growth factor concentrations. RESULTS: Three independent assays demonstrate that VEGF protein is present at substantially elevated levels in a wound fluid associated with the formation of abdominal granulation tissue. However, the wound fluid is not hypoxic at any time. Serial sampling reveals that transforming growth factor beta-1 protein appears in the wound fluid before VEGF. CONCLUSIONS: The results suggest that VEGF is a prominent regulator of wound angiogenesis and vessel permeability. A factor other than hypoxia, perhaps the earlier appearance of another growth factor, transforming growth factor beta-1, may positively regulate VEGF appearance in the wound fluid.     

CCN1 Promotes VEGF Production in Osteoblasts and Induces Endothelial Progenitor Cell Angiogenesis by Inhibiting miR‐126 Expression in Rheumatoid Arthritis

Angiogenesis is the formation of new capillaries from preexisting vasculature. The perpetuation of angiogenesis plays a critical role in the pathogenesis of various disease states including rheumatoid arthritis (RA). Cysteine‐rich 61 (Cyr61 or CCN1) is an important proinflammatory cytokine in RA. Here, we investigated the role of CCN1 in angiogenesis associated with vascular endothelial growth factor (VEGF) production and osteoblasts. We found higher expression of CCN1 and VEGF in synovial fluid from RA patients compared with healthy controls. CCN1 induced VEGF expression in osteoblasts and increased endothelial progenitor cells (EPCs) angiogenesis by inhibiting miR‐126 via the protein kinase C‐alpha (PKC‐α) signaling pathway. CCN1 knockdown inhibited angiogenesis in both in vitro and in vivo models. Inhibition of CCN1 expression with lentiviral vectors expressing short hairpin RNA (shRNA) ameliorated articular swelling, cartilage erosion, and angiogenesis in the ankle joint of mice with collagen‐induced arthritis (CIA). Our study is the first to describe how CCN1 promotes VEGF expression in osteoblasts and increased EPCs angiogenesis in RA disease. CCN1 may serve as a potential target for RA treatment. © 2016 American Society for Bone and Mineral Research.