肝再生中表皮生长因子（EGF）及其受体的作用

肝细胞在正常情况下很少分裂，但在肝损伤后会表现出强大的再生能力。肝细胞的生长和增殖受到众多因子的影响，其中表皮生长因子（Epidermal Growth Factor，EGF）是一种强有丝分裂原，它与受体EGFR结合后能诱导组织细胞的增殖、分化、成熟，是目前已知的能够促进肝脏再生的一个主生长因子。现就表皮生长因子对肝再生的作用做一综述。     

VEGF在妇产科及生殖领域中的应用

血管内皮生长因子(VEGF)是一组功能强大且能产生多种生物学效应的细胞因子,它能够促进血管内皮细胞增殖及体内新生血管形成并增加血管通透性.近年来在女性生殖内分泌领域中VEGF受到相当的重视.本研究就VEGF的生物特性,以及其在妇产科领域、辅助生殖技术中的应用作一综述.     

NF-κB信号通路在大鼠肝再生中调节肝细胞增殖的机理研究

为了解大鼠肝再生中肝细胞NF-κB信号通路对肝细胞增殖的调节作用,用Rat Genome 230 2.0芯片检测大鼠肝再生中NF-κB信号通路相关基因表达变化发现,芯片含138个NF-κB信号通路基因,其中46个基因与大鼠肝再生相关.用Ingenuity Pathway Analysis 9.0(IPA)软件解析上述基因表达变化预示的该信号通路调节肝细胞增殖作用发现,该通路的白细胞介素-1(IL-1)途径在大鼠肝再生起始阶段促进肝细胞增殖,生长因子(GF)途径在进展阶段促进肝细胞增殖,肿瘤坏死因子-α(TNF-α)途径在起始阶段促进肝细胞增殖,终止阶段抑制肝细胞增殖.     

肝再生细胞周期中增殖启动及其调控研究

肝再生细胞周期中增殖启动及其调控是一个研究热点,到底是何种因素及其涉及到的信号传导途径诱导了Go期肝细胞的启动仍然是一个谜.本文主要以JNK、TNF-α、IL-6、一氧化氮等因子及其可能参与的调控途径综述了肝再生启动的一些最新研究进展.     

血管内皮细胞生长因子在损伤修复中的作用

近年研究显示血管内皮细胞生长因子能够促进局部组织的血管化,而血管生成是生理及病理性组织生长和损伤愈合的基础,故血管内皮细胞生长因子在损伤修复中有重要的作用.目前认为这一作用主要是促进内皮细胞有丝分裂和使细胞通透性增强,通过和血管内皮细胞的特异性受体结合,产生强大的促进内皮增殖及血管生成作用而实现的.     

一部颇有学术造诣的力作——《大鼠肝再生的功能基因组学研究》书评

2009年底,中国高等教育出版社出版的《大鼠肝再生的功能基因组学研究》专著,分上、中、下3册,总计530多万字,汇总了大鼠再生肝及包括肝细胞、胆管上皮细胞、卵圆细胞、星形细胞、窦内皮细胞、库普弗细胞、陷窝细胞、树突状细胞等8种细胞在内的肝再生基因组学研究结果,证实8 124个基因与大鼠肝再生相关.本书资料系统、翔实、丰富,有助于了解(肝)再生的复杂性,也有助于经济、高效、有针对性地开展相关研究,是从事再生生物学和再生医学等研究不可多得的工具书和参考书.     

血管内皮细胞生长因子在损伤修复中的作用

近年研究显示血管内皮细胞生长因子能够促进局部组织的血管化,而血管生成是生理及病理性组织生长和损伤愈合的基础,故血管内皮细胞生长因子在损伤修复中有重要的作用。目前认为这一作用主要是促进内皮细胞有丝分裂和使细胞通透性增强,通过和血管内皮细胞的特异性受体结合,产生强大的促进内皮增殖及血管生成作用而实现的。     

肝细胞生长因子（HGF）对肝再生的影响

肝细胞在正常情况下很少分裂，但在肝损伤后会表现出强大的再生能力。肝细胞生长因子（Hepatocyte Growth Factor，HGF）是一个多效应生长因子，参与机体多种器官组织细胞的生长、再生和重塑等过程。但是它在肝再生中所起的作用尤为突出，现就其做一综述。     

桦树皮提取物抑制血管生成作用的研究

研究桦树皮提取物对血管生成的抑制作用.应用MTT法检测桦树皮提取物对人脐静脉内皮细胞的增殖抑制作用,采用Realtime PCR方法检测桦树皮提取物对人脐静脉内皮细胞中VEGFmRNA表达的影响,应用ELISA测定细胞上清液中VEGF的分泌情况.实验表明,桦树皮提取物能显著抑制人脐静脉内皮细胞增殖,最高浓度150 μg/mL其抑制率达48.4%,能明显抑制人脐静脉内皮细胞内VEGFmRNA的表达及VEGF分泌.结果表明桦树皮提取物可通过抑制细胞内VEGF mRNA的表达及VEGF的分泌有效抑制人脐静脉内皮细胞的增殖.     

大鼠连续部分肝切除模型的建立及应用研究

分析在肝细胞去分化时期和再分化时期依次切除大鼠肝的左叶、中叶、右叶、尾叶对大鼠生存的影响,并建立了４种连续部分肝除模型,用这些模型分析了肝再生过程中肝细胞组织结构、细胞核数、有丝分裂指数、核仁大小和数目、增殖细胞核抗原变化发现,损上发的细胞去分化、增殖和再分化,是从激活细胞膜上的碱性磷酸酶开始的提示细胞内可能存在不同于正常条件下细胞增殖调控的途径。     

A peptide fusion protein inhibits angiogenesis and tumor growth by blocking VEGF binding to KDR

Vascular endothelial growth factor (VEGF) binding to its tyrosine kinase receptors (KDR/FLK1, Flt-1) induces angiogenesis. In search of the peptides blocking VEGF binding to its receptor KDR/FLK1 to inhibit tumorangiogenesis and growth, we screened a phage display peptide library with KDR as target protein, and some candidate peptides were isolated. In this study, we cloned the DNA fragment coding the peptide K237 from the library, into a vector pQE42 to express fusion protein DHFR-K237 in E. coli M15. The affection of fusion protein DHFR-K237 on endothelial cell proliferation and angiogenesis was investigated. In vitro, DHFR-K237 could completely block VEGF binding to KDR and significantly inhibit the VEGF-mediated proliferation of the human vascular endothelial cells. In vivo, DHFR-K237 inhibited angiogenesis in chick embryo chorioallantoric membrane and tumor growth in nude mice. These results suggest that K237 is an effective antagonist of VEGF binding to KDR, and could be a potential agent for cancer biotherapy.     

血管内皮生长因子在低氧运动中的效应及一氧化氮的介导作用

血管内皮生长因子(VEGF)是内皮细胞特异性的有丝分裂原,具有促进内皮细胞增生、迁移和增加血管通透性等多种重要生物学作用。研究表明,VEGF在发挥这些生物学作用的过程中一氧化氮(NO)起着必不可少的作用。随着高原训练理论研究的不断深入,低氧运动条件下VEGF对机体机能影响的研究倍受关注,其中VEGF和NO关系的探讨有助于低氧运动状况下对VEGF作用机制的进一步阐述。     

血管内皮生长因子对女性生殖功能的调控及其临床意义

血管内皮生长因子是一种特异性血管生长因子，在血管的发生中发挥重要作用。在卵巢、子宫内膜、胎盘等部位有丰富的VEGF及其受体的表达，对女性生殖功能发挥重要的调控作用。近年来VEGF在妇产科领域的临床研究结果表明，VEGF的异常表达与卵巢癌、妊娠高血压、子宫内膜异位症有着密切的关系。     

电刺激小脑顶核促脑缺血后血管内皮生长因子表达的意义

探讨电刺激小脑顶核(FNS)对局部脑缺血后血管内皮生长因子(VEGF)表达和毛细血管新生的影响．以线栓法制成大鼠右侧大脑中动脉梗塞模型(MCAO)，大鼠随机分为假手术对照组、MCAO组、电刺激小脑顶(MCAO FNS)干预组，以免疫组织化学法检测VEGF、内皮细胞阳性表达及毛细血管记数，大脑中动脉梗塞后，缺血区神经元变性、坏死，VEGF、内皮细胞在半暗带有少量表达，毛细血管数较对照组增加，经电刺激小脑顶核干预后，VEGF、内皮细胞大量表达，毛细血管数目明显增加，有统计学差异．电刺激小脑顶核可通过促VEGF表达、内皮细胞增殖，从而促进毛细血管新生。     

白藜芦醇诱导VEGF表达促进缺血再灌注小鼠新生血管形成

研究白藜芦醇能否诱导小鼠缺血,再灌注后缺血区域新生血管形成及其与血管内皮细胞生长因子(VEGF)表达的相关性,用90只雄性BALB/c小鼠随机分为单纯缺血组、白藜芦醇组及假手术组,采用大脑中动脉线栓法制作局灶性脑缺血模型,免疫组化法测定微血管密度,Western blot检测VEGF蛋白表达.结果白藜芦醇处理组与单纯缺血对照组微血管计数存在差异,并且有统计学意义(P<0. 05),白藜芦醇处理组在各时间点VEGF蛋白表达水平均较高(P<0.05).说明白藜芦醇可以诱导脑缺血后VEGF早期表达,促进缺血区域新生血管形成,发挥脑保护作用.     

Functions of VEGF in female reproductive system

As a homodimeric glycoprotein,vascular endothelial growth factor(VEGF)is a highly specific mitogen of vascular endothelial cells.It can induce proliferation and migration,and inhibit apoptosis of endothelial cell.VEGF is involved in many processes in the female reproductive system,such as ovulation,periodical changes of endometrium,embryo implantation and development,VEGF plays important roles in some reproductive diseases,including preeclampsia and fetal hypoevolutism in uterus.Based on our studies on angiogenesis and its relevant factors in the female reproductive system these years,the functions of VEGF in female reproductive system are reviewed,and the research prospect and application of VEGF are also discussed.     

Homoharringtonine induces apoptosis of endothelium and down－regulates VEGF expression of K562 cells

Homoharringtonine (HHT) has currently been used successfully in the treatment of acute and chronic myeloid leukemias and has been shown to induce apoptosis of different types of leukemic cells in vitro. Emerging evidence suggests that angiogenesis may play an important role in hematological malignancies, such as leukemia. However, whether HHT can relieve leukemia by anti-angiogenesis is still unknown. We investigated the anti-angiogenesis potential of HHT with the human umbilical vein endothelial cell line (ECV304) and leukemic cell line (K562) in vitro. Cellular proliferation was determined by MTT assay and apoptosis was analyzed by flow cytometry, The mRNA expression of vascular endothelial growth factor (VEGF) was assessed by RT-PCR and VEGF protein production was detected by Western blot. Inhibition of cell proliferation and induction of apoptosis by HHT were discovered in ECV304 cells, and appeared in a dose- and time-dependent manner, Also, treatment with HHT caused down-regulation of VEGF mRNA expression in K562 cells in similar dose- and time-dependent manner and inhibition of VEGF protein production in K562 cells in response to the enhancing concentration of HHT. The results demonstrated that HHT could also induce apoptosis in endothelium and down-regulate VEGF expression in K562 cells. In conclusion, we believe HHT has anti-angiogenesis potential and speculate that HHT might exert its anti-leukemia effects via reduction of angiogenesis.     

Notch-dependent VEGFR3 upregulation allows angiogenesis without VEGF-VEGFR2 signalling

Developing tissues and growing tumours produce vascular endothelial growth factors (VEGFs), leading to the activation of the corresponding receptors in endothelial cells. The resultant angiogenic expansion of the local vasculature can promote physiological and pathological growth processes. Previous work has uncovered that the VEGF and Notch pathways are tightly linked. Signalling triggered by VEGF-A (also known as VEGF) has been shown to induce expression of the Notch ligand DLL4 in angiogenic vessels and, most prominently, in the tip of endothelial sprouts. DLL4 activates Notch in adjacent cells, which suppresses the expression of VEGF receptors and thereby restrains endothelial sprouting and proliferation. Here we show, by using inducible loss-of-function genetics in combination with inhibitors in vivo, that DLL4 protein expression in retinal tip cells is only weakly modulated by VEGFR2 signalling. Surprisingly, Notch inhibition also had no significant impact on VEGFR2 expression and induced deregulated endothelial sprouting and proliferation even in the absence of VEGFR2, which is the most important VEGF-A receptor and is considered to be indispensable for these processes. By contrast, VEGFR3, the main receptor for VEGF-C, was strongly modulated by Notch. VEGFR3 kinase-activity inhibitors but not ligand-blocking antibodies suppressed the sprouting of endothelial cells that had low Notch signalling activity. Our results establish that VEGFR2 and VEGFR3 are regulated in a highly differential manner by Notch. We propose that successful anti-angiogenic targeting of these receptors and their ligands will strongly depend on the status of endothelial Notch signalling.     

Identification of an angiogenic mitogen selective for endocrine gland endothelium

The known endothelial mitogens stimulate growth of vascular endothelial cells without regard to their tissue of origin. Here we report a growth factor that is expressed largely in one type of tissue and acts selectively on one type of endothelium. This molecule, called endocrine-gland-derived vascular endothelial growth factor (EG-VEGF), induced proliferation, migration and fenestration (the formation of membrane discontinuities) in capillary endothelial cells derived from endocrine glands. However, EG-VEGF had little or no effect on a variety of other endothelial and non-endothelial cell types tested. Similar to VEGF, EG-VEGF possesses a HIF-1 binding site, and its expression is induced by hypoxia. Both EG-VEGF and VEGF resulted in extensive angiogenesis and cyst formation when delivered in the ovary. However, unlike VEGF, EG-VEGF failed to promote angiogenesis in the cornea or skeletal muscle. Expression of human EG-VEGF messenger RNA is restricted to the steroidogenic glands, ovary, testis, adrenal and placenta and is often complementary to the expression of VEGF, suggesting that these molecules function in a coordinated manner. EG-VEGF is an example of a class of highly specific mitogens that act to regulate proliferation and differentiation of the vascular endothelium in a tissue-specific manner.