胰岛素样生长因子-1对MC3T3-E1细胞增殖及Ⅰ型胶原蛋白合成的影响

目的观察胰岛素样生长因子-1（IGF-1）对体外培养的小鼠前成骨样MC3T3-E1细胞增殖及Ⅰ型胶原蛋白合成的影响,探讨IGF-1对骨代谢可能的影响机制。方法不同浓度rhIGF—1刺激体外培养的MC3T3-E1,用噻唑蓝（MTT）法测定细胞增殖能力。结果一定浓度IGF-1能明显增加戍骨细胞数量（P〈0．05）,在1ng／mL～100ng／ml。这种作用与IGF-1的浓度呈正相关;经rhIGF-1的刺激,成骨细胞Ⅰ型胶原蛋白的表达明显高于对照组（P〈0．05）;半定量RT—PCR显示在rhIGF-1干预48h后,Ⅰ型胶原蛋白mRNA表达较对照组明显增加。结论IGF-1对MC3T3-E1细胞有明显的促增殖作用,在0．1ng／mL～100ng／mL之间呈浓度依赖性,IGF-1能促进成骨细胞Ⅰ型胶原蛋白的合成及其mRNA的表达。     

瘦素促进人肝癌细胞HepG2增殖的初步研究

目的探讨外源性瘦素对人肝癌细胞HepG2生长增殖的影响。方法体外培养HepG2,给予不同浓度瘦素(50ng/ml、100ng/ml、200ng/ml),MTT法观察瘦素对HepG2生长的影响,流式细胞仪检测瘦素对HepG2细胞周期的作用。结果 0ng/ml～200ng/ml瘦素在作用72h内呈现出剂量、时间依赖性地促进HepG2的增殖,不同浓度组之间及不同时间组之间,差异均具有统计学意义(P0.01,P0.01),并且随着瘦素浓度的增加,HepG2G0～G1期细胞比例逐渐下降(P0.01),S期及G2-M期细胞比例逐渐上升(P0.01,P0.01)。结论瘦素在离体实验中具有明显的促进入肝癌细胞HepG2增殖的效应,此效应与促进细胞DNA合成、增强有丝分裂有关,提示瘦素有可能参与肝癌的发生、发展过程。     

榄香烯对PLA801D细胞株诱导分化研究

目的观察榄香烯（elemene）对体外培养的PLA801D细胞株（人肺巨细胞癌株）生长抑制作用。方法应用相差显微镜观察经不同浓度的榄香烯溶液（25、50和100μg/／L）作用的PLA801D细胞形态学改变，流式细胞仪检测细胞凋亡率及细胞周期各时相的变化，电子显微镜观察亚细胞结构改变。结果对照组细胞呈梭形贴壁生长，实验组细胞贴壁不佳，细胞数目变少，细胞改变呈剂量依赖性。流式细胞仪结果显示，G1期细胞增多，S期细胞减少，G2／M期细胞相对增多，电子显微镜下可见细胞核染色质趋边凝集，胞质有空泡。结论榄香烯能够抑制体外培养的PLA801D细胞生长，阻滞PLA801D细胞G1期向S期转化进程，且呈剂量依赖性诱导细胞凋亡。     

神经生长因子抑制肝星状细胞增殖的观察

目的 观察神经生长因子(NGF)对大鼠肝星状细胞(HSC)增殖的抑制作用,并探讨其作用机制. 方法 体外培养大鼠肝星状细胞株HSC-T6,将HSC-T6与不同浓度NGF孵育后,用XTT比色法检测NGF对HSC增殖的影响,流式细胞术分析NGF对HSC细胞周期的影响,透射电镜观察经100 ng/ml NGF作用24h后HSC形态学变化.结果 (100、200、400) ng/ml浓度时NGF对HSC的抑制作用经XTT法测得A值分别为0.66±0.03、0.69±0.03和0.66±0.03,与对照组(0.73±0.01)比较,差异具有统计学意义(P＜0.05),但无浓度依赖性(P＞0.05).100、200、400ng/ml NGF作用于HSC 24h后,G2期比例分别为14.83％±5.41％、14.73％±2.50％和14.87％±2.06％,与对照组(7.47％±4.39％)比较,明显增加(P＜0.05),透射电镜可以见到细胞凋亡的形态学变化. 结论 NGF可抑制HSC增殖,通过使HSC细胞周期停滞于G2期而抑制HSC增殖可能为其作用机制之一;经NGF作用的大鼠肝星状细胞可出现明显的增殖受抑、细胞凋亡的形态学改变.     

结缔组织生长因子及其抗体对人胃成纤维细胞生物学功能的影响

目的 研究结缔组织生长因子(CTGF)及其抗体对人胃成纤维细胞增殖、移行、合成细胞外基质(ECM)的影响.方法 (1)应用四唑盐(MTT)比色法检测不同浓度的CTGF(5、20、50、100 ng/ml)及其抗体(0.1、0.5、1 μg/ml)对人胃成纤维细胞增殖的影响.(2)应用羟脯氨酸法检测不同浓度的CTGF及其抗体对人胃成纤维细胞分泌胶原蛋白的影响.(3)应用Transwell小室法检测不同浓度的CTGF及其抗体对人胃成纤维细胞迁移能力的影响.结果 5 ～ 10 ng/ml CTGF可剂量依赖性地促进入胃成纤维细胞增殖;20～ 100 ng/ml CTGF可剂量依赖性地促进人胃成纤维细胞分泌胶原蛋白;20～ 100 ng/ml CTGF可剂量依赖性地促进人胃成纤维细胞迁移.另一方面,0.1～1μg/ml CTGF抗体可剂量依赖性地抑制人胃成纤维细胞增殖;0.5、1 μg/ml CTGF抗体可剂量依赖性地抑制人胃成纤维细胞分泌胶原蛋白;0.5、1 μg/ml ETGF抗体可剂量依赖性地抑制人胃成纤维细胞迁移.以上各实验组与相应对照组比较均有显著性差异(P＜0.05).结论 一定浓度范围内的CTGF能剂量依赖性地促进人胃成纤维细胞增殖、分泌胶原蛋白及迁移,这表明CTGF参与了胃硬癌间质纤维化进程,在间质纤维化进程的各环节发挥重要作用.而一定浓度范围内的CTGF抗体可剂量依赖性地抑制这些效应,这为胃硬癌的临床治疗提供了新的思路.     

水飞蓟素对雷帕霉素诱导的内皮祖细胞凋亡和生长抑制的拮抗作用

目的:水飞蓟素对雷帕霉素诱导的内皮祖细胞（EPCs）凋亡和生长抑制的拮抗作用。方法:通过密度梯度离心法分离、培养、鉴定得到EPCs;在EPCs培养物中加入不同浓度（0、01、1、10、100 ng/ml）的雷帕霉素干预24 h和加入（1 ng/ml）雷帕霉素干预不同时间（0 、6、12、24、48 h）。收集细胞检测其增殖和迁移能力。在EPCs培养物中加入不同浓度（0、25、50、100 μg/ml）的水飞蓟素干预24 h后,收集细胞检测其增殖、迁移和凋亡的水平。在EPCs培养物中同时加入（1 ng/ml）雷帕霉素和不同浓度（25、50、100 μg/ml）水飞蓟素干预24 h后,收集细胞检测其增殖、迁移、凋亡和体外血管生成的能力。结果:与未药物干预的EPCs培养物相比较,雷帕霉素（1、10、100 ng/ml）能抑制EPCs增殖和迁移,并随干预浓度的增加和干预时间的延长而增加（P<0.05）。水飞蓟素干预24 h后,50 μg/ml和100 μg/ml的水飞蓟素可明显增加EPCs增殖和迁移的能力（P<0.05）,25~100 μg/ml的水飞蓟素可明显抑制EPCs凋亡（P<005）,并呈浓度依赖性。EPCs在加入雷帕霉素（1 ng/ml）和不同浓度水飞蓟素（25、50、100 μg/ml）共同干预24 h后,50 μg/ml和100 μg/ml的水飞蓟素都可明显改善雷帕霉素对EPCs的促凋亡作用,并能逆转雷帕霉素对EPCs增殖、迁移和血管形成能力的抑制作用（P<0.05）。结论:雷帕霉素能抑制EPCs增殖和迁移,并呈浓度和时间依赖性。水飞蓟素能增强EPCs增殖和迁移,抑制其凋亡,并呈浓度依赖性。水飞蓟素能抑制雷帕霉素对EPCs的促凋亡作用,并能逆转雷帕霉素对EPCs增殖、迁移和血管形成能力的抑制作用。     

神经生长因子对肝星状细胞生物行为学的影响

目的 探究神经生长因子(NGF)对肝星状细胞(HSCs)增殖、凋亡的影响及其可能的作用机制.方法 对数生长期HSC-T6细胞随机分为对照组(0 ng/ml)、NGF低剂量组(100 ng/ml)、NGF中剂量组(200 ng/ml)和NGF高剂量组(300 ng/ml),采用CCK-8法检测HSC-T6的增殖情况;采用流式细胞仪检测HSC-T6的凋亡情况;采用逆转录-聚合酶链反应(RT-PCR)检测α-平滑肌肌动蛋白(SMA)、Ⅰ型胶原及基质金属蛋白酶组织抑制因子(TIMP)-1的mRNA表达水平;采用Western印迹检测含半胱氨酸的天冬氨酸蛋白水解酶(Caspase)-3、p53的蛋白表达变化.结果 与对照组比较,NGF低、中、高剂量组的细胞增殖均受到显著抑制,细胞凋亡率则显著增加,且各NGF处理组之间的这种变化呈明显的剂量依赖效应(P<0.05).NGF低、中、高剂量组细胞中α-SMA、Ⅰ型胶原及TIMP-1的mRNA相对表达水平较对照组均显著下调,并且该变化趋势随着NGF剂量的增加而增强(P<0.05).与对照组比较,NGF低、中、高剂量组细胞中Caspase-3、p53的表达水平均显著增加,各NGF剂量组之间的蛋白表达变化具有明显的剂量依赖性(P<0.05).结论 NGF通过调控TIMP-1、Ⅰ型胶原、Caspase-3和p53等基因的表达抑制HSCs的增殖并诱导其凋亡,这可能为肝纤维化的临床治疗开辟新的思路.     

硝普钠对人血管平滑肌细胞合成胶原的抑制作用

目的 探讨内皮素（ET-1）对人血管平滑肌细胞（HVSMC）合成胶原的影响，并观察硝普钠（SNP）对HVSMC合成胶原的影响。方法 将ET-l10^-8mol／L和不同浓度SNP加人体外培养HVSMC。培养24h后测培养液中NO含量，测细胞内cGMP含量及^3H-脯氨酸掺人量即总胶原含量。结果 加入梯度浓度SNP，NO水平呈剂量依赖性增加（均P〈0．01）；ET-1使胶原合成量增加80％（P〈0．01），加入梯度浓度SNP较ET-1组胶原合成量分别减少了38％、42％、57％（均P〈0．01），呈剂量依赖性；ET-1＋SNP低、中、高浓度组较ET-1组细胞内cGMP含量明显增加（均P〈0．01），且cGMP含量随SNP增加而增加；细胞内cGMP含量与胶原合成量呈良好负相关关系（r=-0．93）。结论 ET-1可引起HVSMC合成胶原增多；SNP可剂量依赖地抑制HVSMC合成胶原；SNP对胶原合成的抑制作用可能是通过cGMP途径起作用。     

表皮细胞培养条件的优化

目的探讨生长因子（EGF）在人表皮细胞无血清培养中的作用，寻找较好组合．以期加快表皮细胞成皮。方法选择EGF、胰岛素、霍乱毒素、氢化考的松4个实验因素，每个因素设立4个浓度水平。利用L16（4X4）正交表设计试验，考察不同培养条件对表皮细胞生长情况、克隆形成率的影响。结果EGF在无血清培养中对培养人表皮细胞的生长及增殖有明显促进作用（P〈0．01），在一定范围内（5～20ng／m1）随EGF浓度提高，效应加强；胰岛素浓度在5g／ml时对培养细胞的生长及增殖影响最大；霍乱毒素浓度在4．2ng／ml时作用最好；氢化考的松作用不明显。EGF、胰岛素、霍乱毒素、氢化考的松分别取20ng／ml、5μg／ml、8．4ng／ml、0．2μg／ml浓度时细胞生长及增殖效果最好。结论采用此优化的培养方法，表皮细胞的生长比较迅速，分化不太明显，可保持较旺盛的增殖力。     

霉酚酸对大鼠肺动脉平滑肌细胞增殖的影响

目的 在细胞水平研究霉酚酸对大鼠肺动脉平滑肌细胞增殖的影响.方法 采用生长曲线、甲基噻唑基四唑(MTT)方法、流式细胞仪检测生长细胞数、细胞的存活值、DNA含量,计算G1,S,G2M和增殖指数.结果 除低浓度(100 nmol/L)外,各霉酚酸组(1、10、100μmol/L)生长细胞数均较对照组减少,差异有统计学意义(p<0.01).MTT法检测霉酚酸组细胞的存活值降低,呈剂量依赖性(100 nmol/L～100 μmol/L).霉酚酸组G1期比例增加,S期比例减少:G2M期比例减少,增殖指数降低,呈剂量依赖性.结论 霉酚酸可有效地抑制大鼠肺动脉平滑肌细胞的增殖,主要作用于DNA合成期,并呈剂量依赖性.其有效浓度在临床可应用的范围内.     

槐耳对人胃癌细胞MGC803增殖和凋亡的影响

[目的]观察中药槐耳对胃癌细胞株MGC803增殖和凋亡的影响.[方法]以不同浓度的槐耳（4、8、16、32、64 mg/ml）分别作用于体外培养的人胃癌细胞MGC803,通过MTT法、划痕实验等检测槐耳对MGC803细胞增殖和迁移的作用,倒置显微镜下观察细胞的形态变化,流式细胞仪检测细胞凋亡情况.[结果]MTT实验显示槐耳可抑制MGC803细胞的生长,呈时间及浓度依赖性;显微镜下可观察到细胞肿胀、破裂、呈坏死状;划痕实验显示,4、8 mg/ml槐耳分别作用MGC803细胞,划痕愈合明显慢于对照组,呈剂量依赖关系;流式细胞仪可检测到MGC803细胞凋亡率明显增加,呈时间及浓度依赖性.[结论]槐耳可抑制人胃癌MGC803细胞的迁移,且能通过诱导细胞凋亡的方式有效地抑制人胃癌细胞MGC803的生长.     

转化生长因子β1单克隆抗体干预成纤维细胞增殖的体外研究

目的观察抗转化生长因子β１（ＴＧＦβ１）单克隆抗体对成纤维细胞（ＦＢ）增殖及胶原合成的影响。方法将肺泡巨噬细胞（ＡＭ）培养上清液与Ｌ９２９成纤维细胞株共同孵育,并加入不同剂量ＴＧＦβ１单克隆抗体,用３Ｈ胸腺嘧啶掺入法观察ＦＢ增殖及胶原合成的情况。结果抗ＴＧＦβ１单克隆抗体能够抑制ＡＭ条件上清液引起的ＦＢ增殖,在一定剂量范围内（１０μｇ／ｍｌ）呈剂量效应关系。抑制作用在１０μｇ／ｍｌ时达到最大并使ＦＢ培养上清Ⅳ型胶原的合成减少３２％。结论提示抗ＴＧＦβ１单克隆抗体的应用可能为肺纤维化的治疗提供潜在的新途径。     

棘霉素诱导肝癌SMMC7721细胞凋亡的研究

目的研究棘霉素诱导肝癌SMMC7721细胞凋亡的作用,探讨其抗肿瘤的作用机制。方法通过细胞计数获得不同浓度棘霉素作用SMMC7721细胞的生长抑制率,观察棘酶素对肝癌细胞生长的影响;通过流式细胞仪分析棘霉素对细胞凋亡和细胞周期的影响。结果棘霉素浓度〉10 ng/ml时可抑制SMMC7721细胞的生长。结论棘霉素在体外可诱导肝癌细胞凋亡,具有很强的抗肿瘤作用。     

Nerve growth factor displays stimulatory effects on human skin and lung fibroblasts, demonstrating a direct role for this factor in tissue repair

Nerve growth factor (NGF) is a polypeptide which, in addition to its effect on nerve cells, is believed to play a role in inflammatory responses and in tissue repair. Because fibroblasts represent the main target and effector cells in these processes, to investigate whether NGF is involved in lung and skin tissue repair, we studied the effect of NGF on fibroblast migration, proliferation, collagen metabolism, modulation into myofibroblasts, and contraction of collagen gel. Both skin and lung fibroblasts were found to produce NGF and to express tyrosine kinase receptor (trkA) under basal conditions, whereas the low-affinity p75 receptor was expressed only after prolonged NGF exposure. NGF significantly induced skin and lung fibroblast migration in an in vitro model of wounded fibroblast and skin migration in Boyden chambers. Nevertheless NGF did not influence either skin or lung fibroblast proliferation, collagen production, or metalloproteinase production or activation. In contrast, culture of both lung and skin fibroblasts with NGF modulated their phenotype into myofibroblasts. Moreover, addition of NGF to both fibroblast types embedded in collagen gel increased their contraction. Fibrotic human lung or skin tissues displayed immunoreactivity for NGF, trkA, and p75. These data show a direct pro-fibrogenic effect of NGF on skin and lung fibroblasts and therefore indicate a role for NGF in tissue repair and fibrosis.     

Taurine chloramine inhibition of cell proliferation and cytokine production by rheumatoid arthritis fibroblast-like synoviocytes

OBJECTIVE: To examine whether taurine (Tau) or its physiologic chlorinated derivative, taurine chloramine (Tau-CI), affects proliferation of, and proinflammatory cytokine (interleukin-6 [IL-6] and IL-8) production by, fibroblast-like synoviocytes (FLS) isolated from rheumatoid arthritis (RA) patients. METHODS: FLS, isolated from the synovial tissue of 19 RA patients and cultured in vitro for 3-6 passages, were stimulated with the recombinant human cytokines IL-1beta (1 ng/ml), tumor necrosis factor alpha (TNFalpha; 10 ng/ml), or IL-17 (10 ng/ml) in the presence of either Tau or Tau-Cl, which were added at concentrations of 50-500 microM. Tau and Tau-Cl were added simultaneously with, 2 hours before, or 24 hours after the stimuli. The concentrations of IL-6 and IL-8 were determined in culture supernatants using specific enzyme-linked immunosorbent assays. Proliferation of FLS was estimated on the basis of 3H-thymidine incorporation into the cells, which were cultured for 72 hours in the presence of recombinant human basic fibroblast growth factor (bFGF) (1 ng/ml) and Tau or Tau-Cl, which were added simultaneously at the beginning of the culture. RESULTS: Cultured in vitro, RA FLS spontaneously secreted low levels of IL-6 and IL-8, but when RA FLS were stimulated with IL-1beta, TNFalpha, or IL-17, significantly higher amounts of IL-6 and IL-8 were produced. Tau-Cl, but not Tau, inhibited cytokine-triggered synthesis of IL-6 (50% inhibitory concentration [IC50] approximately 225 microM) and IL-8 (IC50 approximately 450 microM) when added simultaneously with the stimuli. However, IL-17-induced production of IL-8 was not affected by Tau-Cl. In the cells prestimulated with IL-1beta for 24 hours, Tau-Cl still inhibited synthesis of IL-6, but did not affect IL-8 production. Moreover, Tau-Cl inhibited spontaneous and bFGF-triggered proliferation of FLS in a dose-dependent manner. Neither Tau nor Tau-Cl affected cell viability. CONCLUSION: The results of these studies demonstrate that Tau-Cl inhibits production of proinflammatory cytokines by RA FLS, as well as proliferation of these cells. Thus, Tau-Cl may act as a physiologic modulator of FLS functions related to their pathogenic role in RA.     

Human eosinophils regulate human lung- and skin-derived fibroblast properties in vitro: A role for transforming growth factor β (TGF-β)

Eosinophils have been associated with fibrosis. To investigate their direct role in fibrosis, human peripheral blood eosinophil sonicate was added to human lung or dermal fibroblasts, and proliferation ([(3)H]thymidine) and collagen synthesis ([(3)H]proline) were evaluated. Proliferation was enhanced significantly in the monolayers in a dose-dependent manner. The activity of the eosinophil fibrogenic factor(s) remained unaltered when heated (56 degrees C, 30 min). Supernatants of cultured eosinophils (20 min or 18 hr) also enhanced lung fibroblast proliferation, indicating that the preformed mitogenic factor(s) can be released both promptly and with a long kinetic. Eosinophils significantly decreased collagen production in lung fibroblasts while increasing it in dermal fibroblasts. However, eosinophils containing matrix metalloproteinase 9 (zymography) in latent form and tissue inhibitors of metalloproteinases 1 and 2 (reverse zymography) did not influence either fibroblast matrix metalloproteinases or tissue inhibitors of metalloproteinases. Eosinophil sonicate added to skin and lung fibroblasts in tridimensional collagen lattices significantly enhanced lattice contraction. Transforming growth factor beta (TGF-beta) is a major fibrogenic cytokine produced by eosinophils. Therefore, to assess its role, eosinophil sonicate was preincubated with anti-TGF-beta neutralizing antibodies. This treatment partially inhibited proliferation of lung and collagen synthesis of dermal fibroblasts and suppressed the stimulation of lattice contraction, indicating the fibrogenic role of eosinophil-associated TGF-beta. In conclusion, we have shown that eosinophils act as direct modulatory cells in fibroblast proliferation, collagen synthesis, and lattice contraction, in part, through TGF-beta. These data corroborate the importance of eosinophils in skin and lung fibrosis.     

Effects of basic fibroblast growth factor, transforming growth factor-beta and nerve growth factor on the secretory function of the bovine corpus luteum in vitro.

The effects were investigated of basic fibroblast growth factor (bFGF), transforming growth factor-beta (TGF-beta) and nerve growth factor (NGF) on the release of progesterone and oxytocin from the bovine corpus luteum (CL) at different stages of the oestrous cycle. A microdialysis system (MDS) of CL and a cell culture system with a reduced number of endothelial cells were used. In the MDS of CL from the mid-luteal stage (days 8-12 of the oestrous cycle), infusion with bFGF (0.1, 1, 10 and 100 ng/ml), TGF-beta (0.1, 1 and 10 ng/ml) and NGF (0.1, 1, 10 and 100 ng/ml) for 30 min induced significant acute effects on the release of progesterone. Both bFGF and NGF stimulated the release of progesterone during peptide infusion, TGF-beta and also bFGF in the period thereafter. This stimulation was dose-dependent during and after the infusion only for bFGF. This response pattern was observed at all luteal stages for the three growth factors, but bFGF was more stimulatory at the early (days 5-7) and mid-luteal stages during and after peptide infusion. The release of oxytocin was stimulated by bFGF in a dose-dependent manner. At the highest dose, bFGF, TGF-beta and NGF stimulated the release of oxytocin throughout all three luteal stages. When luteal cells were cultured with growth factors, only TGF-beta showed a dose-dependent inhibition of both basal and LH-stimulated progesterone as well as oxytocin release (measured between 48 and 52 h of culture). NGF had an inhibitory effect only on the basal release of oxytocin. bFGF had no effect on the release of either hormone under continuous stimulation in cell culture. The results indicate that bFGF, TGF-beta and NGF act directly and acutely on the secretory function of bovine CL in the MDS but also have long-term effects as shown in cell culture. bFGF appears to be an important autocrine/paracrine regulator of CL function, since local expression of its mRNA, peptide synthesis and its mitogenic and non-mitogenic actions have now been confirmed. Endothelial cells from the CL have been identified as target cells for bFGF. Differences observed between the two systems might thus be attributed to the presence or absence of cell-to-cell contact and a reduced number of endothelial cells, as well as to the duration of peptide stimulation and medium changes every 24 h compared with the flow-through conditions in the MDS.     

血小板衍生生长因子—BB对血管内皮细胞、平滑肌细胞及成纤维细胞增殖的影响

目的 观察血小板衍生生长因子—BB对培养的人血管内皮细胞、兔平滑肌细胞和人成纤维细胞增殖的影响。方法 采用培养的人脐静脉血管内皮细胞、兔动脉血管平滑肌细胞和人血管成纤维细胞，应用^3H—TdR掺入方法，观察血小板衍生生长因子—BB对三种细胞DNA合成的影响。结果 血小板衍生生长因子—BB可促进处于静止状态的三种细胞DNA的合成，并呈现出明显的浓度依赖关系，在30ng／ml的浓度时成纤维细胞DNA的合成达到高峰，在40ng／ml的浓度时内皮细胞、平滑肌细胞DNA的合成达到高峰。成纤维细胞、平滑肌细胞分别在PDCF-BB作用24h和36h年到DNA合成的高峰，内皮细胞在48h时DNA合成量最高。结论 血小板衍生生长因子—BB可明显促进培养的人脐静脉血管内皮细胞、兔动脉血管平滑肌细胞和人血管成纤维细胞的增殖。     

The cell-adhesive effect of basic fibroblast growth factor on pituitary cells in vitro

Both native and recombinant basic fibroblast growth factor (FGF) exerted a marked effect on the morphology of a pituitary clonal somatotroph-like cell line (MtT/S) in vitro. Addition of 10 pg-20 ng bovine basic FGF/ml caused the cells to flatten and spread out over the culture dish, the cells showing strong surface contact. Those in contact with the culture dish were epithelial in appearance, being polygonal, closely apposed and forming a pavement-like monolayer. Basic FGF inhibited cell proliferation in a dose-dependent manner at the higher concentrations tested (0.5-20 ng/ml). This cell-adhesive effect of basic FGF was also observed in normal dispersed pituitary cells. The observed stimulation of pituitary cell adhesion is the first report of a morphological effect of basic FGF on pituitary cells and could explain the physiological significance of basic FGF and its high concentration in the pituitary gland.