退变腰椎间盘组织中碱性成纤维细胞生长因子的表达研究

目的 探讨碱性成纤维细胞生长因子（basic fibroblast growth factor,bFGF)在正常和退变椎间盘组织中的表达情况。方法 交30例来源于腰椎间盘突出症患者手术中所取得的椎间盘组织（观察组，男11例，女19例；年龄25－78岁，平均48岁；病程3个月－30年，平均9年11个月）与6例来源于脊柱侧凸患者前路松解术所取得的椎间盘组织（对照组，男女各3例，年龄10－17岁，平均14.2岁）进行对比，首先经病理组织学检查证实为退变椎间盘组织和政党椎间盘组织，然后将两组椎间盘组织分别通过免疫组织化学方法和原位杂交方法，检测各自椎间盘组织中的bFGF及其mRNA的表达。观察组30例均为退变椎间盘组织，免疫组化阳性率为90％（27／30），原位杂交阳性率为20％（6／30）；对照组6例均为正常椎间盘组织，其免疫组及原位杂交均为阴性，两组间免疫组化方法检测阳性率在统计学上差异有非常显著性意义。结论 bFGF在正常和退变椎间盘组织中表达的差异有显著性意义。提示 bFGF可能作为增生刺激因子促进椎间盘组织中的软骨细胞增生和细胞外基质合成，进而加速椎间盘退变。     

肾母细胞瘤组织中碱性成纤维细胞生长因子和纤维细胞生长因子受体表达分析

肾母细胞瘤 (ＮＢＴ)是婴幼儿泌尿系最常见的恶性肿瘤。我们采用ＲＴ ＰＣＲ技术对ＮＢＴ组织中碱性成纤维细胞生长因子 (ｂＦＧＦ)和纤维细胞生长因子受体 (ＦＧＦＲ)基因进行定量分析 ,探讨其临床意义。资料与方法　 38例ＮＢＴ标本、2 2例肾癌癌旁组织标本 ,均经病理学诊断证实为ＮＢＴ。患儿年龄 1～ 3岁。实验方法 :总ＲＮＡ提取。ｂＦＧＦ、ＦＧＦＲ引物由北京奥科生物有限公司合成。引物序列采用ｐｒｉｍｅｒｐｒｅｍｉｅｒ 5 .0软件处理系统设计 ,并以 β ａｃｔｉｎ为内参照。ＲＴ ＰＣＲ试剂购自大连宝生物有限公司 ,采用 2 0 μ…     

碱性成纤维细胞生长因子对成骨细胞中转化生长因子-β1和碱性成纤维细胞生长因子mRNA表达的影响

目的　探讨外源性碱性成纤维细胞生长因子 (bFGF)对体外成骨细胞中的生长因子 :转化生长因子 β1 (TGF β1 )和bFGFmRNA表达的影响。 方法　将体外培养的新生SD大鼠颅骨成骨细胞 ,用不同浓度的bFGF(5～ 50 μg/L)进行处理 ,利用核酸原位分子杂交 ,检测两种生长因子在细胞中mRNA的表达。结果　依bFGF浓度的增加成骨细胞内TGF β1mRNA表达分别是对照组的 1 .5、1 .6、1 .9和 2 .0倍 ;bFGFmRNA表达则分别是对照组的 1 .2 8、1 .37、1 .40和 1 .51倍。bFGF组中 ,TGF β1和bFGFmRNA的表达量均明显高于对照组 (P <0 .0 1 )。结论　外源性bFGF可以对成骨细胞自分泌bGFG产生影响 ,还能够促进TGF β1的合成     

碱性成纤维细胞生长因子在肌腱组织工程中的应用

目的综述近年来碱性成纤维生长因子（basic fibroblast growth factor，bFGF）在组织工程肌腱相关研究中的进展。方法广泛杏阅同内外相关文献，进行整理、综合与分析。结果bFGF在促进组织工程肌腱标准细胞系的建立，诱导支架材料的合成与降解，增强细胞与支架材料之间的相互作用，加速组织工程材料的再血管化等方面均有明显作用。结论促进内源性bFGF合成、控释外源性bFGF及提高bFGF的生物利用度等方面取得的进展，为bFGF在组织工程中的应用开辟厂良好的应用前景。     

膀胱癌中碱性成纤维细胞生长因子的研究现状

碱性成纤维细胞生长因子是一种具有多功能的促有丝分裂原 ,研究已表明其参与恶性肿瘤的形成过程。近年来 ,碱性成纤维细胞生长因子在膀胱癌发病过程中的作用、与生物学行为之间关系以及治疗上的应用已受到重视     

P物质对大鼠成纤维细胞碱性成纤维细胞生长因子及其受体表达的影响

目的　探讨P物质 (SP)对大鼠肉芽组织成纤维细胞碱性成纤维细胞生长因子 (bF GF)及其受体 (FGFR 1)表达的影响。方法　采用成纤维细胞体外培养和逆转录 多聚酶链反应(RT PCR)技术 ,观察SP在不同浓度 ( 1× 10 - 9～ 1× 10 - 5mol L)及孵育时间 ( 0、3、6、12、2 4h)情况下刺激成纤维细胞后 ,其bFGF、FGFR 1mRNA表达情况。结果　SP可上调大鼠成纤维细胞bF GF、FGFR 1mRNA表达。SP对bFGF的量 效曲线呈双相分布 ,最大效应浓度为 1× 10 - 7mol L。但SP仅在高浓度 ( 1× 10 - 6 ～ 1× 10 - 5mol L)时促进FGFR 1表达。在最大效应浓度 ( 1× 10 - 7～ 1× 10 - 5mol L)时 ,SP对bFGF、FGFR 1表达的上调作用分别于刺激细胞后 3、12h达高峰。结论　SP对大鼠肉芽组织成纤维细胞bFGF、FGFR 1基因表达存在直接影响 ,其表现形式与SP的刺激浓度及孵育时间有关 ,这可能是SP在创伤修复中发挥作用的机制之一。     

碱性成纤维细胞生长因子在卵巢上皮性肿瘤中的表达及意义

目的 探讨碱性成纤维细胞生长因子（ｂＦＧＦ）在卵巢上皮性肿瘤的生物学行为中的作用。方法 应用免疫组织化学对１０例正常卵巢组织和８０例卵巢上皮性肿瘤进行对照研究,同时应用Ｍｉａｓ－２００图像分析系统进行定量分析,并研究恶性肿瘤中ｂＦＧＦ的表达强度与临床分期以及肿瘤类型和病理分级间的关系。结果 （１）ｂＦＧＦ主要在卵巢上皮性肿瘤细胞浆内表达,在交界型和恶性肿瘤中,部分阳性细胞同时存在细胞核表达。（２）     

异体肾移植慢性排斥组织中病变血管bFGF及PDGFR的表达及意义

目的：探讨bFGF及PDGFR的表达与同种异体肾移植慢性排斥反应血管病变之间的关系。方法：采用免疫组织化学SP法研究23例排斥肾组织、12例正常肾组织、14例远离癌的正常肾组织血管中bFGF及PDGFR的表达。结果：bFGF及PDGFR在排斥组织血管平滑肌细胞、内膜层的表达明显高于正常及癌旁组织，差异有显著性意义，其中内膜层的差异较平滑肌层更为明显。结论：bFGF及PDGFR的表达可调控正常血管组织，过度表达与肾移植慢性排斥反应血管病变密切相关。     

碱性成纤维细胞生长因子在退变椎间盘组织中表达的研究进展

近年来由于CT、MRI等影像学新技术的广泛应用，人们发现在椎间盘突出症患者中，存在着突出椎问盘组织的吸收或缩小现象，研究表明生化机制可能在椎间盘退变中起着更重要的作用，并发现碱性成纤维细胞生长因子(bFGF)可促进体内、外软骨细胞增生和细胞外基质合成，影响椎间盘退变，这方面的研究国内报道较少。现将bFGF在椎间盘组织中的表达研究作一综述。     

碱性成纤维细胞生长因子在肾癌中的表达及意义

目的：探讨碱性成纤维细胞生长因子（b-FGF)在肾癌中的表达及意义。方法：采用斑点杂交技术测定20例肾癌患者癌组织,癌旁和周围正常肾组织中b-FGF mRNA的表达情况。结果：肾癌组织中b-FGF mRNA明显高于癌旁和周围正常肾组织（P＜0．01）,b-FGF mRNA的升高与肿瘤分期和分级密切相关,与肿瘤大小无明显关系。结论：b-FGF在肾癌组织中自身分泌,与肾癌的发生和发展密切相关。     

bFGF及PDGFR表达与肾移植慢性排斥血管病变和肾小球损？…

目的 探讨碱性成纤维细胞生长因子（ｂＦＧＦ）及血小板源性生长因子受体（ＰＤＧＦＲ）的表达与肾移植慢性排斥反应血管病变及肾小球损伤之间的关系。方法 采用免疫组化ＳＰ法检测２３例排斥肾组织、１２例正常肾组织、１４例远离癌的正常肾组织血管及肾小球中ｂＦＧＦ及ＰＤＧＦＲ的表达。结果 ｂＦＧＦ及ＰＤＧＦＲ在排斥组织血管平滑肌细胞、内膜层及肾小球中的表达明显高于正常组织及癌组织（Ｐ〈均０．０１）。结论 ｂＦＧ     

Vascular endothelial growth factor expression in human chronic renal allograft rejection

BACKGROUND: Chronic renal allograft rejection is characterized by interstitial fibrosis and vasculopathy. Vascular endothelial growth factor (VEGF) is an endothelial mitogen with increased expression in inflammation and vasculopathy. METHODS: Renal tissue from 17 patients with chronic rejection was examined for VEGF protein and the presence of CD 68-positive macrophages, and compared to biopsies from patients with temporary allograft dysfunction, acute rejection, and native kidneys with thin membrane disease. RESULTS: In the chronic rejection group, there was markedly increased expression of VEGF protein in the interstitium (P<0.0001). In serial sections, VEGF colocalized with the expression of CD 68-positive macrophages. Significantly more macrophages were in the tubulointerstitium in tissue with chronic rejection than in those with temporary allograft dysfunction (P<0.005). Additionally, VEGF protein expression in the glomeruli and the vascular compartment of patients with chronic rejection was increased. CONCLUSION: The up-regulation of VEGF in chronic renal allograft rejection may be important in inflammation and development of fibrosis.     

SDF-1 expression is elevated in chronic human renal allograft rejection

The exact mechanism of acute and chronic allograft rejection still remains unclear. The chemokine SDF-1 as mediator of allograft rejection has been under intensive investigation in liver, cardiac and bone marrow transplantation, whereas in renal transplantation, there are no reports about SDF-1 to date. This study was performed to evaluate if SDF-1 might also play an important role in human renal graft biopsies. One hundred and ninety formalin-fixed, paraffin-embedded renal allograft biopsies were included in the analysis from patients with normal renal graft morphology (according to Banff 97 classification grade 1, n = 84), with acute interstitial rejection (Banff grade 4 type I, n = 10), with acute vascular rejection (Banff grade 4 type II, n = 21), with chronic allograft nephropathy (CAN, Banff grade 5, n = 23), and without rejection but with various other lesions (Banff grade 6, n = 42). SDF-1 was localized by immunohistochemistry. In biopsies with CAN, SDF-1 expression was significantly elevated in interstitial infiltrates and infiltrating neointimal cells of arteries compared with biopsies with normal renal graft morphology. This is the first study describing a role of SDF-1 in human renal allograft rejection. We were able to demonstrate in a large number of biopsies an upregulation of SDF-1 in patients with CAN. Whether SDF-1 has pro-inflammatory or protective properties in this setting has to be evaluated in further trials.     

移植肾慢性排斥组织中血小板源性生长因子受体表达研究

目的探讨生长因子在同种异体肾移植慢性排斥反应肾组织中的表达、分布及临床意义。方法采用免疫组化ＳＰ法研究１２例正常肾、１４例肾癌旁及２３例慢性排斥肾组织中血小板源性生长因子受体（ＰＤＧＦＲ）表达。结果排斥肾组织ＰＤＧＦＲ表达阳性率为９１％，明显高于正常组织及癌旁组织（２５％，２８％），差异有显著性，ＰＤＧＦＲ主要表达于血管平滑肌、肾小球膜、肾小管等细胞的胞浆、胞膜及核膜。结论ＰＤＧＦＲ表达可调控正常肾组织，高表达与慢性排斥密切相关；未发现ＰＤＧＦＲ表达与临床症状相关。     

Early prognosis of the development of renal chronic allograft rejection by gene expression profiling of human protocol biopsies

BACKGROUND: Chronic allograft rejection (CR) is the major cause of failure of long-term graft survival and is so far irreversible. Early prognosis of CR by molecular markers before overt histologic manifestation would be a valuable aid for the optimization of treatment regimens and the design of clinical CR trials. Oligonucleotide microarray-based approaches have proven to be useful for the diagnosis and prognosis of a variety of diseases and were chosen for the unbiased identification of prognostic biomarkers. METHODS: Renal allograft biopsies were taken at month 6 posttransplantation (PT) from two groups who were, at that time, healthy recipients: one group developed CR at month-12 PT, the other group remained healthy. Gene expression profiles from the two groups at month-6 PT biopsies were analyzed to identify differentially expressed genes with prognostic value for CR development at month 12. RESULTS: A set of 10 genes was identified that showed differential expression profiles between the two patient groups and had a complete separation of the 15% to 85% quantile range for each individual gene. This set of genes was sufficient to allow the correct prediction of the occurrence or nonoccurrence of CR in 15 of 17 (88%) patients using cross-validation (occurrence for a patient was predicted on the basis of the other patients' data only). In addition, a correct prediction could be made that a recipient with a normal biopsy 12 months PT developed CR within the following 6 months. CONCLUSIONS: Identified expression patterns seem to be highly prognostic of the development of renal CR.     

C4d complement split product expression in chronic rejection of renal allograft

Chronic allograft rejection remains the major cause of late renal graft loss. Its pathogenesis is complex, depending on both immunological and nonimmunological factors. An important role in development of chronic rejection is ascribed to an ongoing immunological reaction mainly of the humoral type. C4d complement split product, as a stable fragment of complement degradation activated by antigen-antibody complexes, is considered to be an indicator of humoral activity in allografts. The aim of the present study was to establish a correlation between C4d expression and morphological findings specific for chronic rejection among biopsy specimens from patients with deteriorating graft function versus protocol biopsy specimens versus biopsy specimens of native kidneys with glomerular diseases. C4d deposits in peritubular capillaries and glomeruli were observed in 83% of patients with morphological changes of chronic rejection. No C4d expression was found in the protocol biopsy group. C4d deposits in glomeruli localizations were found in kidneys from patients with glomerulopathies; the pattern of distribution was similar to that for antibodies characteristic for glomerulonephritis. There was a positive correlation between C4d expression and morphological features of chronic rejection. In our opinion, only peritubular capillary localization is specific for a rejection process; glomerular localization is nonspecific and probably secondary to antigen-antibody complex deposition in course of some types of glomerulopathies.