CD151蛋白激活Rac/Cdc42通路并促进血管生成

目的研究CD151及其突变体CD151-AAA194-196对人脐静脉内皮细胞(HUVEC)增殖及激活Rac/cdc42通路的影响,探讨CD151促血管生成的机制。方法构建pAAV-CD151及其突变体pAAV-CD151-AAA194-196(整合素结合缺陷突变体),测序成功后分别转染入HUVEC。CCK-8法测定pAAV-CD151及其突变体pAAV-CD151-AAA194-196在HUVEC中增殖的能力,Western Blot方法检测CD151及突变体转染后CD151蛋白的表达及对激活Rac/Cdc42通路的影响。结果 pAAV-CD151组的CD151蛋白表达高于正常对照组、pAAV-GFP组,但pAAV-CD151组及pAAV-CD151-AAA194-196组之间CD151蛋白表达没有统计学意义(P>0.05)。CCK-8检测结果示:Control组、pAAV-GFP组、pAAV-CD151组、pAAV-CD151-AAA194-196组OD值分别为1.491±1.780、1.403±1.776、2.742±2.49和1.66±1.845。pAAV-CD151组较pAAV-GFP组和Control组细胞增殖能力明显增强(P<0.01),pAAV-CD151-AAA194-196组较pAAV-CD151组细胞增殖能力减弱(P<0.05)。此外,pAAV-CD151组中P-Rac/cdc42表达较pAAV-GFP组和正常对照组明显增加(P<0.01),pAAV-CD151-AAA194-196组较pAAV-CD151组P-Rac/cdc42表达降低(P<0.05)。结论 CD151通过与整合素形成功能性复合体机制促进Rac/Cdc42通路的激活,进而促进血管生成作用。上述机制可能为CD151促血管生成的重要机制。     

CD34+和CD34-细胞在NOD/SCID小鼠体内的造血重建

利用非肥胖糖尿病型重症联合免疫缺陷型(NOD/SCID)小鼠模型, 比较了新鲜及培养后的CD34+和CD34-细胞在体内植入及重建造血能力。从新鲜脐血及培养后的单个核细胞(MNC)中分离出CD34+和CD34-细胞, 经尾静脉输注入经亚致死剂量照射的NOD/SCID小鼠体内, 6周后处死存活的小鼠, 取其骨髓、脾脏和外周血细胞, 分别进行细胞表型分析、造血集落形成单位和人特异性基因的检测。经检测, 输注CD34+细胞和混合细胞的小鼠, 其体内CD45+细胞及人源各系血细胞的含量相近, 两者均远远高于输注CD34-细胞的小鼠。输注培养后CD34-细胞的小鼠饲养6周后全部死亡,输注培养后CD34+细胞的小鼠存活率约为66.7%, 而输注培养后混合细胞的小鼠全部存活, 且在两组存活的小鼠体内均能检测到CD45+细胞及人源各系血细胞。结果表明: 无论是新鲜还是培养后的CD34+细胞均具有在NOD/SCID小鼠体内植入和重建造血能力, 而CD34-细胞不具有该能力, 但CD34-细胞与CD34+细胞同时输注有助于提高小鼠的存活率, 说明其对CD34+细胞在小鼠体内发挥植入和造血重建能力有一定的辅助作用。     

Uptake and intracytoplasmic storage of pigmented particles by human CD34+ stromal cells/telocytes: endocytic property of telocytes

We studied the phagocytic‐like capacity of human CD34+ stromal cells/telocytes (TCs). For this, we examined segments of the colon after injection of India ink to help surgeons localize lesions identified at endoscopy. Our results demonstrate that CD34+ TCs have endocytic properties (phagocytic‐like TCs: phTCs), with the capacity to uptake and store India ink particles. phTCs conserve the characteristics of TCs (long, thin, bipolar or multipolar, moniliform cytoplasmic processes/telopodes, with linear distribution of the pigment) and maintain their typical distribution. Likewise, they are easily distinguished from pigment‐loaded macrophages (CD68+ macrophages, with oval morphology and coarse granules of pigment clustered in their cytoplasm). A few c‐kit/CD117+ interstitial cells of Cajal also incorporate pigment and may conserve the phagocytic‐like property of their probable TC precursors. CD34+ stromal cells in other locations (skin and periodontal tissues) also have the phagocytic‐like capacity to uptake and store pigments (hemosiderin, some components of dental amalgam and melanin). This suggests a function of TCs in general, which may be related to the transfer of macromolecules in these cells. Our ultrastructural observation of melanin‐storing stromal cells with characteristics of TCs (telopodes with dichotomous branching pattern) favours this possibility. In conclusion, intestinal TCs have a phagocytic‐like property, a function that may be generalized to TCs in other locations. This function (the ability to internalize small particles), together with the capacity of these cells to release extracellular vesicles with macromolecules, could close the cellular bidirectional cooperative circle of informative exchange and intercellular interactions.     

Up-regulation of miR-210 by vascular endothelial growth factor in ex vivo expanded CD34+ cells enhances cell-mediated angiogenesis

Ex vivo culture has been proposed as a means to augment and repair autologous cells in patients with chronic diseases, but the mechanisms governing improvement in cell function are not well understood. Although microRNAs (miRs) are increasingly appreciated as key regulators of cellular function, a role for these factors in CD34+ cell-mediated angiogenesis has not been elucidated. Vascular endothelial growth factor (VEGF) was previously shown to induce expression of certain miRs associated with angiogenesis in endothelial cells and promote survival and number of vascular colony forming units of haematopoietic stem cells (HSCs). We sought to evaluate the role of VEGF in expansion and angiogenic function of CD34+ cells and to identify specific miRs associated with angiogenic properties of expanded cells. Umbilical cord blood CD34+ cells were effectively expanded (18- to 22-fold) in culture medium containing stem cell factor (SCF), Flt-3 ligand (Flt-3), thrombopoietin (TPO) and interleukin-6 (IL-6) with (postEX/+VEGF) and without VEGF (postEX/noVEGF). Tube formation in matrigel assay and tissue perfusion/capillary density in mice ischaemic hindlimb were significantly improved by postEX/+VEGF cells compared with fresh CD34+ and postEX/noVEGF cells. MiR-210 expression was significantly up-regulated in postEX/+VEGF cells. MiR-210 inhibitor abrogated and 210 mimic recapitulated the pro-angiogenic effects by treatment of postEX/+VEGF and postEX/noVEGF cells respectively. Collectively, these observations highlight a critical role for VEGF in enhancing the angiogenic property of expanded cells, and identify miR-210 as a potential therapeutic target to enhance CD34+ stem cell function for the treatment of ischaemic vascular disease.     

Regulation of cell shape and adhesion by CD34

We previously reported that expression of CD43/leukosialin induces cell rounding and microvillus formation via inhibition of cell adhesion. Here, we found that CD34, a cell surface sialomucin and marker for hematopoietic progenitor cells, also inhibited cell adhesion and induced cell rounding and microvillus formation. Forced expression of CD34-induced cell rounding, microvillus formation, and phosphorylation of ezrin/radixin/moesin (ERM) proteins in HEK293T cells, while inhibiting integrin-mediated cell re-attachment. Furthermore, CD34+ blood cells and KG-1 cells, which express endogenous CD34 on their surface, were spherical in shape, surrounded by microvilli, and non-adherent to substrata. In addition, cleavage of O-sialomucin augmented integrin-mediated cell adhesion of KG-1 cells. These results suggest the involvement of CD34 in the inhibition of integrin-mediated cell adhesion and formation of the cell surface structure. The inhibitory function of CD34 in cell adhesion may affect cell shape organization via phosphorylation of ERM proteins. Cellular structures such as the spherical shape and microvilli of CD34+ cells may also contribute to regulation of cell adhesion.     

Persistence of CD34 Stem Marker in Human Lipoma: Searching for Cancer Stem Cells

Background: Lipomas are benign solid tumours that develop in soft tissues with origin in mesenchymal progenitors. Macroscopically, they appear as soft-elastic nodules, varying in volume from a few millimiters to several centimetres and can enlarge progressively. Although they are usually asymptomatic, they can cause symptoms due to nerve or vessel compression. Microscopically they appear as fibrous connective tissue stroma with embedded adipocytes, and absence of inflammation. Up to now no characterisation of stem cell population present in this tissue has been performed.Methods: Cytofluorimetric, biological and molecular biology analyses have been performed in order to test superficial cell markers and gene expression profile related to stemness and apoptotic activity of cells present in lipoma tissues compared to those of adipose tissue''s cells.Results: Our results confirmed that CD34⁺ cells in lipoma were present around small adipocytes, showing several altered biological activity such as proliferation, apoptotis and stemness.Conclusions: The data emerging from the comparison of the lipoma cells and normal adipose tissue, suggests the presence of cell precursors involved in the development of the lipoma. This hypothesis requires further investigation and may indicate new thresholds in the study of benign tumour pathogenesis.     

Phenotypic variability and therapeutic implications of Candida species in patients with oral lichen planus

We investigated the prevalence and phenotypic variation of Candida species in oral lichen planus (OLP) and the therapeutic implications of our findings. Eighty patients with clinically and histopathologically confirmed cases of OLP (64 non-erosive, 16 erosive) and a control group of 80 healthy individuals with no predisposing factors for oral candidiasis were examined for evidence of Candida infection. Oral swabs and smears were obtained for cytology and culture. Identification, speciation and antifungal susceptibility tests of Candida isolates were performed using an automated microbial identification system. Fifty percent of erosive OLP cases, 28% of non-erosive cases and none of the controls showed evidence of Candida. Candida albicans was found predominantly in non-erosive OLP, while other Candida species were predominate in erosive OLP. Non-Candida albicans isolates (C. glabrata, C. krusei) were resistant to the commonly used antifungals, clotrimazole and fluconazole. Candida infection is common in cases of OLP. We recommend antifungal sensitivity testing prior to antifungal therapy for the erosive form of OLP.     

Detection and identification of non-Candida albicans species in human oral lichen planus

Candida species were detected and identified in samples from the buccal mucosa, dorsal surface of the tongue and supragingival plaque of subjects with oral lichen planus (OLP). The Candida in the samples were cultured on selection agars, and identified by sequence analyses of 18S, 5.8S and 25/28S rRNA. The isolation frequency of Candida was higher in subjects with OLP than in those with healthy oral mucosa. Non-C. albicans were only isolated from people with OLP. These results support the notion that subjects with OLP are more likely to have oral colonization with Candida, and that non-C. albicans are specifically present in subjects with this condition.     

Stimulation of immune suppressive CD34+ cells from normal bone marrow by Lewis lung carcinoma tumors

 Progressive growth of metastatic Lewis lung carcinoma (LLC-LN7) tumors is associated with increased levels of bone-marrow-derived CD34⁺ cells having natural suppressor (NS) activity toward T cells. The present studies determined whether tumor-derived products are responsible for this induction of NS activity. Culturing normal bone marrow cells with LLC-LN7-conditioned medium (LLC-CM) or with recombinant granulocyte/macrophage-colony-stimulating factor (GM-CSF) resulted in the appearance of NS activity. The development of NS activity coincided with a prominent increase in the levels of CD34⁺ cells. That the CD34⁺ cells were responsible for the NS activity of the bone marrow cultures containing LLC-CM was shown by the loss of NS activity when CD34⁺ cells were depleted. The stimulation of CD34⁺ NS cells by LLC-CM was attributed to tumor production of GM-CSF, since neutralization of GM-CSF within the LLC-CM reduced its capacity to increase CD34⁺ cell levels. Studies also showed that the induction of CD34⁺ NS cells by LLC-CM and GM-CSF could be overcome by including in the cultures an inducer of myeloid differentiation, 1α,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃]. These results demonstrate that the mechanism by which the LLC-LN7 tumors stimulate increased levels of CD34⁺ NS cells from normal bone marrow is by their production of GM-CSF and that this can be blocked with the myeloid differentiation inducer 1,25(OH)₂D₃. Received: 8 December 1997 / Accepted: 27 February 1998     

De novo protein sequencing,humanization and in vitro effects of an antihuman CD34 mouse monoclonal antibody

QBEND/10 is a mouse immunoglobulin lambda-chain monoclonal antibody with strict specificity against human hematopoietic progenitor cell antigen CD34. Our in vitro study showed that QBEND/10 impairs the tube formation of human umbilical vein endothelial cells (HUVECs), suggesting that the antibody may be of potential benefit in blocking tumor angiogenesis. We provided a de novo protein sequencing method through tandem mass spectrometry to identify the amino acid sequences in the variable heavy and light chains of QBEND/10. To reduce immunogenicity for clinical applications, QBEND/10 was further humanized using the resurfacing approach. We demonstrate that the de novo sequenced and humanized QBEND/10 retains the biological functions of the parental mouse counterpart, including the binding kinetics to CD34 and blockage of the tube formation of the HUVECs.     

血小板生成素诱导胎肝CD34~ 造血干/祖细胞增殖分化与周期蛋白表达的关系

为了解胚胎时期巨核细胞增殖分化特有的内在机制 ,本研究观察了在体外培养体系中 ,胎肝源CD3 4 造血干 /祖细胞在血小板生成素 (thrombopoietin ,TPO)作用下增殖分化特征与相关周期蛋白B1、D1和D3表达及细胞内水平变化的关系。结果发现 :( 1)经 12d培养后 ,TPO使胎肝源CD3 4 细胞数从 1× 0 5个细胞 /ml增加到 13 12± 4 0 6× 10 5个细胞 /ml,CD4 1 细胞增加到了 95 % ,CD3 4 细胞下降到了 3 % ,大部分细胞的DNA倍性为 2N ,少数为 4N ,无大于 4N巨核细胞 ,TPO对MegaCultTm C胶原半固体培养体系中胎肝源CD3 4 细胞形成CFU Mk集落产率的影响呈明显的剂量效应关系 ;( 2 )在整个培养期间 ,周期蛋白B1表达逐渐增加 ,并保持在一个高水平上 ,培养后期 ,高水平的周期蛋白B1出现在G1期细胞上 ;( 3 )周期蛋白D1和D3表达先增加 ,培养后期细胞内水平下降 ,且以G2期细胞为主。该结果提示 :( 1)TPO通过上调周期蛋白B1和在所有细胞周期时限上调周期蛋白D1和D3表达 ,促进巨核细胞祖细胞的增殖分化 ;( 2 )周期蛋白B1在G2 M期的持续高水平和周期蛋白D1和D3在G2 M期的水平下降 ,可能导致胎肝源巨核细胞核内有丝分裂延迟或阻滞。     

S-亚硝基谷胱甘肽诱导脐带血CD34+细胞来源的巨核细胞产生血小板

为了探讨一氧化氮供体S-亚硝基谷胱甘肽（S—nitrosoglutathione,GSNO）对脐带血CD34^＋细胞分化来源的巨三核细胞产生血小板的可能作用,我们采用免疫磁珠法从8例健康产妇足月顺产的胎儿脐带血中分选CD34^＋细胞,并在含血小板生成素（thrombopoietin,TPO,50ng／ml）、白细胞介素-3（IL-3,10ng／ml）、干细胞因子（stem cell factor,SCF,50ng／ml）和重组人粒-巨噬细胞刺激因子（rHu GM—CSF,20ng／ml）的无血清培养基中培养14d。随后,用免疫磁珠法分选CD61^＋细胞。CD61^＋细胞在含有（实验组）和缺乏（对照组）GSNO（20mg／ml）的无血清培养基[含TPO（50ng／ml）、IL-3（10ng／ml）、SCF（50ng／ml）]中培养不同时间（30min、2h）。采用流式细胞仪检测培养体系中的血小板数;电子显微镜观察巨核细胞的形态学;倒置显微镜和流式细胞仪观察凝血酶诱导的血小板凝集;ELISA方法检测巨核细胞中cGMP的含量。结果显示,与对照组比较,实验组血小板数量明显增加（P〈0．05）;电子显微镜下可见巨核细胞有明显伪足形成和突出;凝血酶诱导后在倒置显微镜和流式细胞仪上均可观察到血小板凝集现象;GSNO作用后巨核细胞中的cGMP明显升高（P〈0．05）。这些结果提示,GSNO可以促进脐带血CD34^＋细胞来源的巨核细胞产生具有一定功能的血小板,其产生的机制可能部分与cGMP途径有关。     

CD117、CD34、DOG-1、WT-1 在胃肠道间质瘤中的表达及意义

目的:探讨DOG-1、CD117、CD34、WT-1在胃肠道间质瘤(GIST)中的表达及临床意义。方法:应用免疫组织化学SP法检测DOG-1、CD117、CD34、WT-1在39例GIST患者肿瘤组织中的表达。结果:GIST光镜下主要由梭形细胞和(或)上皮样细胞或多形性细胞混合或单一性组成。DOG-1、CD117、CD34和WT-1在GIST肿瘤组织中阳性表达率分别为92.3%(36/39)、71.7%(28/39)、64.1%(25/39)、23.1%(9/39),四者的阳性表达率在各风险程度组(极低及低度危险性GIST、中度危险性GIST、高度危险性GIST)两两比较中差异均无统计学意义(P>0.05)。DOG-1与CD117相比,在极低及低度危险组中表达有显著差异(P<0.05),DOG-1与CD34相比,在极低及低度危险组、高度危险组中表达有显著差异(P<0.05);WT-1与CD117相比,在中度及高度危险组中表达有显著差异(P<0.05),WT-1与CD34相比,在中度危险组中表达有显著差异(P<0.05)。对照组平滑肌瘤、纤维瘤、神经鞘瘤中CD117、DOG-1在GIST中的表达明显高于其他多种梭形细胞的表达(P<0.05)。结论:DOG1是GIST较为敏感和特异的标记物,WT-1在极低及低度危险性GIST中有一定的诊断价值,在GIST的诊断中加入两者将使患者更加受益。     

Glomerular CD34 expression in short- and long-term diabetes.

Aging and diabetes are associated with exacerbated expression of adhesion molecules. Given their importance in endothelial dysfunction and their possible involvement in the alteration of glomerular permeability occurring in diabetes, we have evaluated expression of the sialomucin-type adhesion molecule CD34 in renal glomerular cells of normal and diabetic animals at two different ages by colloidal gold immunocytochemistry and immunoblotting. CD34 labeling was mostly assigned to the plasma membranes of glomerular endothelium and mesangial processes. Podocyte membranes were also labeled, but to a lesser degree. Short- and long-term diabetes triggers a substantial increase in immunogold labeling for CD34 in renal tissues compared with young normoglycemic animals. However, the level of labeling in old diabetic and healthy control rats is similar, suggesting that the effect of diabetes and aging on CD34 expression is similar but not synergistic. Western blotting of isolated glomerular fractions corroborated immunocytochemical results. Increased expression of CD34 may reflect its involvement in the pathogenesis of glomerular alterations related to age and diabetes. Alterations present in early diabetes, resembling those occurring with age, strengthen the concept that diabetes is an accelerated form of aging.     

CD34 Class III positive cells are present in atherosclerotic plaques of the rabbit model of atherosclerosis

CD34 is a positive marker for haematopoietic stem cells and endothelial cells. Recent evidence suggests that haematopoietic progenitor cells are involved in atherogenesis. CD34-positive haematopoietic progenitor cells have never been described in rabbit atherosclerotic tissues. The aim of this study is to identify CD34-positive haematopoietic progenitor cells in rabbit atherosclerotic tissues, and to compare this with macrophage (RAM-11), alpha smooth muscle cell actin and fibroblast (prolyl-4-hydroxylase) immunoreactive cells. Sixteen Male New Zealand White rabbits were divided into two groups: Group 1, control diet (Con); group 2, 0.5% cholesterol diet, and killed after 12 weeks. Immunohistochemistry was used to detect CD34 haematopoietic progenitor cells. CD34-positive haematopoietic progenitor cells were identified both within and overlying atherosclerotic plaques. As well, these haematopoietic progenitor cells also stained for RAM-11, CD45, prolyl-4 hydroxylase and alpha smooth muscle cell actin. These findings suggest that in the rabbit model of atherosclerosis, the previously identified macrophages, smooth muscle cells and fibroblasts within and overlying atherosclerotic plaques might be of haematopoietic origin.     

A familiar stranger:CD34 expression and putative functions in SVF cells of adipose tissue

Human adipose tissue obtained by liposuction is easily accessible and an abundant potential source of autologous cells for regenerative medicine applications. After digestion of the tissue and removal of differentiated adipocytes, the so-called stromal vascular fraction (SVF) of adipose, a mix of various cell types, is obtained. SVF contains mesenchymal fibroblastic cells, able to adhere to culture plastic and to generate large colonies in vitro , that closely resemble bone marrow-derived colony forming units-fibroblastic, and whose expanded progeny, adipose mesenchymal stem/stromal cells (ASC), show strong similarities with bone marrow mesenchymal stem cells. The sialomucin CD34, which is well known as a hematopoietic stem cell marker, is also expressed by ASC in native adipose tissue but its expression is gradually lost upon standard ASC expansion in vitro . Surprisingly little is known about the functional role of CD34 in the biology and tissue forming capacity of SVF cells and ASC. The present editorial provides a short introduction to the CD34 family of sialomucins and reviews the data from the literature concerning ex- pression and function of these proteins in SVF cells and their in vitro expanded progeny.     

Hypoxic regulation of angiotensin-converting enzyme 2 and Mas receptor in human CD34+ cells

CD34⁺ hematopoietic stem/progenitor cells (HSPCs) are vasculogenic and hypoxia is a strong stimulus for the vasoreparative functions of these cells. Angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1–7)/Mas receptor (MasR) pathway stimulates vasoprotective functions of CD34⁺ cells. This study tested if ACE2 and MasR are involved in the hypoxic stimulation of CD34⁺ cells. Cells were isolated from circulating mononuclear cells derived from healthy subjects (n = 46) and were exposed to normoxia (20% O₂) or hypoxia (1% O₂). Luciferase reporter assays were carried out in cells transduced with lentivirus carrying ACE2- or MasR- or a scramble-3′-untranslated region gene with a firefly luciferase reporter. Expressions or activities of ACE, angiotensin receptor Type 1 (AT1R), ACE2, and MasR were determined. In vitro observations were verified in HSPCs derived from mice undergoing hindlimb ischemia (HLI). In vitro exposure to hypoxia-increased proliferation and migration of CD34⁺ cells in basal conditions or in response to vascular endothelial growth factor (VEGF) or stromal-derived factor 1α (SDF) compared with normoxia. Expression of ACE2 or MasR was increased relative to normoxia while ACE or AT1R expressions were unaltered. Luciferase activity was increased by hypoxia in cells transfected with the luciferase reporter plasmids coding for the ACE2- or MasR promoters relatively to the control. The effects of hypoxia were mimicked by VEGF or SDF under normoxia. Hypoxia-induced ADAM17-dependent shedding of functional ACE2 fragments. In mice undergoing HLI, increased expression/activity of ACE2 and MasR were observed in the circulating HSPCs. This study provides compelling evidence for the hypoxic upregulation of ACE2 and MasR in CD34⁺ cells, which likely contributes to vascular repair.     

β-ME和BHA体外诱导人胎肝CD34+细胞向神经组织细胞分化研究

目的:建立巯基乙醇(β-mercaptoethanol,β-ME)和丁羟回醚(butylated hydroxyanisole,BHA)体外诱导人胎肝(fetal liver,FL)干细胞向神经细胞分化模型.方法:采用MACS试剂盒分离人胚胎肝CD34 细胞,以DMEM 10%胎牛血清培养液培养;第五代细胞待细胞融合达80%后,用DMEM 10%胎牛血清 1mmol/L β-ME 0.2 mmol/L BHA诱导24 h,PBS洗涤.然后在无血清培养基中培养5 h～5 d.用免疫细胞化学方法分析诱导前后的细胞表型特点.结果:经β-ME BHA诱导处理后,细胞表现神经元样细胞形态,表达神经组织细胞特异蛋白,如neustin、NeuN、NF-M、TuJ-1和NSE.统计显示81%细胞NeuN染色阳性,75%细胞TuJ-1染色阳性,47%染色NF-M阳性,90%染色NSE阳性.结论:β-ME和BHA能够诱导体外培养的人FL CD34 细胞分化为具有神经细胞特异性抗原和成分的神经样细胞;胚胎肝细胞具有向神经组织分化的潜能.     

VEGF、CD34、VEGF—C和VEGFR-3在胃癌中的表达及临床意义

目的：探讨胃癌组织中VEGF、CD34、VEGF-C和VEGFR-3的表达情况及临床意义。方法：采用免疫组化方法测定81例胃癌组织VEGF、CD34、VEGF—C和VEGFR-3表达情况,并结合患者的临床病理资料进行分析。结果：81例胃癌组织中MVD平均值为（42.95±14．79）个／视野,范围为13．00-68．33个／视野,VEGF、VEGF—C、VEGFR-3阳性表达率分别为74．1％、64．2％、67．9％。VEGF的表达与肿瘤的TNM分期、浸润深度、淋巴结转移有关,CD34的表达与肿瘤的分化程度、TNM分期、浸润深度、淋巴结转移有关,VEGF—C的表达与肿瘤的分化程度、浸润深度、淋巴结转移有关,VEGFR-3的表达与肿瘤的浸润深度、淋巴结转移有关。结论：VEGF、CD34、VEGF—C和VEGFR-3的表达与胃癌的浸润转移密切相关。