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1.
脑创伤组织提取液对培养星形胶质细胞的形态特征及FOS基因… 总被引:1,自引:0,他引:1
本研究应用分子杂交和形态学方法观察脑创伤组织提取液对培养大鼠脑星形胶质细胞c-fos原癌基因表达的影响及形态特征改变。发现在分散培养7d后换置于含有脑创伤组织提取液的培养液30 ̄60min,斑点杂交显示星形胶质细胞c-fos原癌基因表达比加正常脑组织提取液组明显,2h后表达减弱。统计学表明有显著差异。推测损伤因素引起了c-fos原癌基因表达,当将脑创伤组织提取液加入新生鼠星形胶质细胞培养液3d后, 相似文献
2.
本研究用分子杂交技术观察了白细胞介素-1β及肿瘤坏死因子-α对脑损伤后及培养的胶质细胞c-fos mRNA表达的影响。结果发现:脑损伤后损伤周围组织c-fos mRNA表达呈动态变化;1h后增加170%,12h后增加30%,24h后增加130%。发现白细胞介素-1β和肿瘤坏死因子-α能显著增加脑损伤后12h及24h c-fos mRNA的表达;当培养的胶质细胞中加入此二者后1h c-fos mRN 相似文献
3.
缺氧对血脑屏障细胞分泌组织型纤溶酶原激活物的影响 总被引:4,自引:0,他引:4
目的:探讨缺氧对体外培养鼠脑微血管内皮细胞和星形胶质细胞分泌组织型纤溶酶原激活物(tissue-type plasminogen activator,TPA)的影响。方法:分别对新生小鼠脑微血管内皮细胞、星状胶质细胞进行缺氧条件下培养,常规培养作为空白对照,每组各取8例,吸取培养液用酶联免疫吸附试验测试TPA活性。结果:缺氧后内皮细胞TPA活性明显增高(P<0.01),星形胶质细胞TPA活性无明显变化(P>0.05)。结论:体外培养鼠脑微血管内皮细胞和星形胶质细胞均能合成分泌TPA;缺氧状态下脑微血管内皮细胞产生的TPA活性增高。内皮细胞分泌的TPA是脑缺氧缺血致不可逆神经元损伤的一个重要媒介,而星形胶质细胞分泌的TPA则主要参与发育阶段需要细胞迁移的重建活动。 相似文献
4.
为了解原癌基因对胎盘滋养层细胞的影响,用原癌基因c-fos、p53蛋白的抗体和运动神经诱向因子1(motoneuronotrophicfactor1,MNTF1)抗独特型抗体的免疫组织化学技术,研究了c-fos、p53及MNTF1受体在人早期胎盘的分布。人早期胎盘的两类滋养层细胞及绒毛中轴的基质细胞均呈c-fos、p53免疫反应性,反应产物大部分布于胞核内。在相邻切片上,c-fos免疫反应性细胞同样显示MNTF1受体免疫反应性,其反应物质分布于胞质内。以上结果提示,原癌基因c-fos和p53可能参与调控绒毛细胞的增殖分化,而且c-fos和MNTF1受体可能有协同调控作用。 相似文献
5.
本实验用免疫组织化学方法观察了L型钙通道激动剂BayK8644皮下注射后小鼠中枢神经系统原癌基因c-fos的表达特点。结果表明,给BayK8644后1/2hc-fos的表达产物Fos蛋白在前嗅核、嗅结节、梨状皮质、齿状回、感觉运动皮质、丘脑室旁核、大脑视皮质纹状区、颞叶听区、中缝核群等区域出现,给药后2~4h表达达高峰,之后进行性消退,16h恢复正常水平。使用钙通道拮抗剂nimodipine对BayK8644所致的Fos表达有拮抗作用。结果提示BayK8644诱导的Fos表达与L型钙通道在脑内的分布较为一致。对Fos和CaBP进行双标记显示,在被观察的脑区Fos/CaBP双标细胞在CaBP免疫反应细胞中的比例约占60.42%~72.88%,c-fos和CaBP的共存是否提示这种细胞同时含有L型钙通道 相似文献
6.
原癌基因c-fos在人早期胎盘绒毛的分布及周龄变化新宇黄威权孙岚(第四军医大学)本文用免疫组织化学ABC法,研究了原癌基因c-fos在人早期胎盘绒毛的分布及周龄变化。免疫组织化学法显示:胎盘绒毛的细胞滋养层细胞、合体滋养层细胞和基质细胞均呈c-fo... 相似文献
7.
对重组转化生长因子β1(TGF-β1)诱导前单核白血病细胞系THP-1细胞向巨噬细胞分化过程中核内原癌基因表达的动态变化进行了研究。结果发现,在诱导分化过程中不同的原癌基因表达变化不仅具有时序性,调节方式也呈多样性。c-fos、c-junmRNA表达变化在时间上有一致性,诱导分化早期(24小时)贴壁细胞的表达量明显增加,延长rhTGP-β1作用时间至48~72小时时,这种上调作用消失,回复到对照组THP-1细胞原有的或低于原有的表达水平。c-myc在细胞分化过程中表达逐渐降低,作用72小时时表达量不足对照组细胞的10%。而c-sis在rhTGP-β1作用72小时内未发现其表达被调节。提示c-fos、c-jun基因在分化早期的表达上调,以及c-myc基因在分化中期的表达被强烈抑制可能分别在分化进程中发挥重要作用。 相似文献
8.
为了解原癌基因对胎盘滋养层细胞的影响,用原癌基因c-fos、p53蛋白的抗体和运动神经诱向因子抗独特特异抗体的免疫组织化学技术,研究了c-fos、p53及MFTF1受体在人早期胎盘的分布。人早期胎盘的两类滋养层主绒毛中轴的基质细胞均呈c-fos、p53免疫反应性,反应产物大部分布于胞核内,在相邻切片上,c-fos免疫反应性细胞同样显示MNTF1受体免疫反应性,其反应物质分布于胞质内。以上结果提示, 相似文献
9.
红藻氨酸致大鼠脊髓损伤过程中c—fos mRNA和Fos的表达变化 总被引:2,自引:0,他引:2
为探讨即早反应基因在神经损伤过程中的变化规律,用原位分子杂交和PAP免疫组织化学方法观察了大鼠脊髓内注射红藻氨酸后1h至14d的不同时间点,L1-3脊髓腹,背角神经元中c-fos mRNA和Fos免疫阳性信号的变化。结果表明,KA致脊髓损伤后2-8h脊髓腹角运动神经元中c-fos mRNA的表达和Fos免疫组织化学阳性反应明显增加,12h恢复至正常水平,伤后3d又明显增强;而脊髓背角神经元内仅在伤 相似文献
10.
SOMAN诱发惊厥后c—fos在大鼠杏仁核簇一氧化氮神经元中的表达 总被引:1,自引:0,他引:1
运用FOS免疫组化结合NADPH-d组化双重标记技术,研究了soman诱发惊厥大鼠杏仁核内c-fos高表达神经地与NADPH-d阳性神经元之间的关系。结果显示;在soman诱发惊后的1.5和48h,杏仁核族凤c-fos呈现持纽过度表达。FOS免疫阳性神经元的分布具有显著的亚核定位特征。 相似文献
11.
目的研究原代大鼠星形胶质细胞氧糖剥夺不同时间miR-21的表达,探讨miR-21是否参与了缺氧缺血性脑损伤后星形胶质细胞的活性变化。方法原代大鼠星形胶质细胞随机分为正常组和氧糖剥夺组,分别培养3、6、9和12h。CCK-8法检测各组星形胶质细胞的活力,real-time PCR方法检测各组星形胶质细胞miR-21的表达。结果氧糖剥夺组miR-21的表达水平随培养时间延长呈先升高后降低的动态变化,3h开始高于对照组水平(P<0.05),6h达高峰(P<0.05),随后下降,9h与对照组无差异(P>0.05),12h显著低于对照组(P<0.05)。氧糖剥夺不同时间星形胶质细胞活力变化与miR-21的变化趋势一致。结论 miR-21可能参与了缺氧缺血性脑损伤后星形胶质细胞的活性变化,发挥促增殖和抗凋亡的作用。 相似文献
12.
目的 观察红细胞生成素激活的星形胶质细胞条件培养液(EACM)对神经干细胞促分化作用及对分化后细胞的保护作用。 方法 原代培养神经干细胞和1型星形胶质细胞,收集红细胞生成素(EPO)刺激的星形胶质细胞上清液,用于神经干细胞分化实验的研究。对分化后的细胞进行免疫细胞化学染色,计算其分化为神经元的比率;同时利用FeSO4和H2O2制造细胞损伤模型,用EACM继续培养48h,然后检测细胞活性和存活细胞数。 结果 EACM组神经干细胞分化明显,神经元比率较星形胶质细胞上清组和对照组均有明显增加。分化后的细胞中加入H2O2后,继续用EACM培养的实验组吸光度(A)值和细胞存活百分比均较对照组高。 结论 红细胞生成素激活的星形胶质细胞条件培养液对神经干细胞有促其向神经元分化的作用,并对分化后的细胞有保护作用。 相似文献
13.
星形神经胶质细胞对PC12细胞生长发育的影响 总被引:8,自引:0,他引:8
在神经系统的生长发育过程中 ,星形胶质细胞对神经元生长发育的作用是一项重要的研究课题。本文以体外培养的 SD大鼠大脑皮质星形胶质细胞与 PC12神经元按不同细胞数目比例 ( 5 0∶ 1~ 1∶ 1)共同培养 ,并用其制备的条件培养液培养 PC12细胞 ,用快速灵敏的 MTT比色法测定 PC12神经元的细胞活力 ,用光学相差显微镜观察 PC12细胞形态学变化。结果显示 ,星形胶质细胞条件培养液可增强 PC12细胞活力 ( MTT测定的 OD值由 0 .2 5 5± 0 .0 12提高到 0 .5 10± 0 .0 3 6,P<0 .0 0 1,且细胞折光性较对照组强 ) ,却不能促使 PC12神经元突起的生出。将星形胶质细胞与 PC12细胞按 3 0∶ 1~ 1∶ 1的比例共同培养时 ,既可提高 PC12细胞折光性和光晕又可促使其突起的生长 ;如按 5 0∶ 1~ 40∶ 1的比例共同培养时 ,只观察到提高 PC12细胞折光性和光晕 ,而无促使其突起生长发育的作用。本文结果提示 ,PC12神经元细胞活力的提高与星形胶质细胞分泌到条件培养液中的可溶性因子有关 ,而 PC12神经元突起生长发育可能是和与星形胶质细胞的直接接触以及二者的细胞数目比有关。 相似文献
14.
ABSTRACT: BACKGROUND: Reactive astrogliosis is a ubiquitous but poorly understood hallmark of central nervous system pathologies such as trauma and neurodegenerative diseases. In vitro and in vivo studies have identified proinflammatory cytokines and chemokines as mediators of astrogliosis during injury and disease; however, the molecular mechanism remains unclear. In this study, we identify astrocyte elevated gene-1 (AEG-1), a human immunodeficiency virus 1 or tumor necrosis factor alpha-inducible oncogene, as a novel modulator of reactive astrogliosis. AEG-1 has engendered tremendous interest in the field of cancer research as a therapeutic target for aggressive tumors. However, little is known of its role in astrocytes and astrocyte-mediated diseases. Based on its oncogenic role in several cancers, here we investigate the AEG-1-mediated regulation of astrocyte migration and proliferation during reactive astrogliosis. METHODS: An in vivo brain injury mouse model was utilized to show AEG-1 induction following reactive astrogliosis. In vitro wound healing and cell migration assays following AEG-1 knockdown were performed to analyze the role of AEG-1 in astrocyte migration. AEG-1-mediated regulation of astrocyte proliferation was assayed by quantifying the levels of cell proliferation markers, Ki67 and proliferation cell nuclear antigen, using immunocytochemistry. Confocal microscopy was used to evaluate nucleolar localization of AEG-1 in cultured astrocytes following injury. RESULTS: The in vivo mouse model for brain injury showed reactive astrocytes with increased glial fibrillary acidic protein and AEG-1 colocalization at the wound site. AEG-1 knockdown in cultured human astrocytes significantly reduced astrocyte migration into the wound site and cell proliferation. Confocal analysis showed colocalization of AEG-1 to the nucleolus of injured cultured human astrocytes. CONCLUSIONS: The present findings report for the first time the novel role of AEG-1 in mediating reactive astrogliosis and in regulating astrocyte responses to injury. We also report the nucleolar localization of AEG-1 in human astrocytes in response to injury. Future studies may be directed towards elucidating the molecular mechanism of AEG-1 action in astrocytes during reactive astrogliosis. 相似文献
15.
P Leprince J M Rigo P P Lefebvre B Rogister P Delrée G Moonen 《Neuroscience letters》1989,102(2-3):268-272
A low-molecular weight astrocyte-derived neuronotoxic activity (ANTA) was detected, using a colorimetric bioassay of cell survival, by its effect on cultured granule cells. This neuronotoxic activity was found to be released rapidly from newborn rat astrocytes in culture upon incubation in 50 mM K+-containing growth medium. The release by astrocytes could be induced repetitively by successive incubations in high-K+ medium alternating with incubations in normal medium. Astrocytes were also found to inactivate rapidly isobutanol-extracted ANTA in normal K+-containing growth medium. Kinetic studies showed that ANTA induces a slow (greater than 12 h) degeneration of cultured granule cells. ANTA is shown here to be an intermediate of normal astrocyte metabolism and to display appropriate kinetic characteristics compatible with its proposed role in inducing part of the delayed neuronal loss that occurs after a brain injury (secondary neuronal death). 相似文献
16.
It is believed that ramified resting microglial cells in the brain are differentiated from macrophage-like ameboid cells, although the mechanism for the differentiation is not fully understood. In the present study, we investigated whether the differentiation of microglial cells is observable in mixed brain cell culture prepared from newborn rat forebrains. In confluent mixed brain cell culture, both ramified and ameboid microglial cells were simultaneously present. The ramified cells were located in or under the astrocyte monolayer, while the ameboid cells were over the layer as revealed by confocal laser scan microscopy. The majority of ramified cells appeared after the astrocyte layer was completely formed and they downregulated the expression of the major histocompatibility complex antigen. Fibronectin was detected around ramified microglial cells, and laminin was also present in the astrocyte monolayer in mixed brain cell culture, while both proteins were not distributed near ameboid cells over the monolayer. When purified microglial cells were cultured on astrocyte-derived extracellular matrix in serum-free medium, they ramified. These results show that the differentiation of microglial cells is observable in culture and that astrocytes may play pivotal roles in the differentiation mainly by secreting insoluble factors. 相似文献
17.
A Kinoshita K Yamada E Kohmura T Hayakawa 《APMIS : acta pathologica, microbiologica, et immunologica Scandinavica》1990,98(9):851-857
To clarify whether astrocyte-derived factors may protect cerebral tissue from ischemia, we examined brain edema, demyelination and astrocyte proliferation in brains with focal ischemia and treated with astrocyte-cultured medium. We occluded the left middle cerebral artery of rats and implanted the Osmotic Minipump, which continuously infused the glial-cultured medium or control medium into the left lateral ventricle. Animals were sacrificed at 3 days or 7 days after occlusion. Brains of both groups were compared by several markers, i.e. extravasation of Evans blue, demyelination by Woelcke's staining and glial proliferation by GFAP staining. We found the astrocyte-cultured medium reduced leakage of Evans blue-plasma protein complex from ischemic lesions and reduced the size of demyelinated lesions. However, the degree of astrocyte proliferation was similar in both groups. From these data, we speculate that humoral factors derived from cultured astrocytes lessened the brain edema by modifying the blood-brain barrier. These factors might also induce proliferation of the microglia, and may protect the neurons from secondary injury by oxygen-free radicals. 相似文献
18.
本研究用分子杂交技术观察了白细胞介素-1β及肿瘤坏死因子-α对脑损伤后及培养的胶质细胞c-fosmRNA表达的影响。结果发现:脑损伤后损伤周围组织c-fosmRNA表达圣动态变化:1h后增加170%.12h后增加30%,24h后增加130%。发现白细胞介素-1β和肿瘤坏死因子-α能显著增加脑损伤后12h及24hc-fosmRNA的表达;当培养的胶质细胞中加入此二者后1hc-fosmRNA表达明显增加,12h后有所下降。又发现同时加入此二者时,c-fosRNA表达增加更加显著。以上结果提示;白细胞介素-1β和肿瘤坏死因子-α能影响脑损伤后胶质细胞c-fosmRNA的表达,它们对胶质细胞的作用可能与c-fos基因有关。 相似文献
19.
新生大鼠大脑皮质O-2A祖细胞的体外诱导分化 总被引:6,自引:0,他引:6
目的 在获取高纯度O 2A祖细胞的基础上 ,探讨O 2A祖细胞在体外分化的形态学特点。方法 采用“两次恒温摇床振荡法”和差速贴壁法 ,结合使用神经营养因子 (bFGF、PDGF AA) ,进行O 2A祖细胞体外纯化和扩增培养 ,并观察O 2A祖细胞在有血清和无血清培养条件下的分化情况 ,用免疫细胞化学鉴定分化成熟的 2型星型胶质细胞和少突胶质细胞。结果 培养的O 2A祖细胞能形成克隆球 ,具有增殖能力 ,经免疫细胞化学鉴定细胞纯度达 90 %以上。在含血清的培养基中能定向分化为 2型星形胶质细胞 ,其胞体较大 ,从胞体上伸出细长突起 ,由突起上再发出更为细小的分支 ,GFAP和A2B5抗体标记均为阳性 ;在无血清的化学条件培养基中能定向分化为少突胶质细胞 ,其胞体较小 ,突起短而细 ,相互交织呈“蜘蛛网”样 ,CNPase抗体标记阳性。结论 (1)培养的O 2A祖细胞保持定向干细胞的特性 ,具有增殖和双向分化的潜能 ;(2 )O 2A祖细胞定向分化为 2型星形胶质细胞过程中经历较长的增殖期 ,而分化为少突胶质细胞过程中则增殖期较短 ;(3)分化的 2型星形胶质细胞和少突胶质细胞在形态学和抗原表达上存在差异。 相似文献
20.
Interferon-gamma induces the expression of immediate early genes c-fos and c-jun in astrocytes.
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N Rubio 《Immunology》1997,91(4):560-564
The expression of the proto-oncogenes, c-fos and c-jun, in cultured mouse astrocytes and its induction by the potent astrocyte activator interferon-gamma (IFN-gamma), were examined by Northern blot and flow cytometry. Both proto-oncogenes were induced in a dose-dependent manner, peaking around 100 U/ml of IFN-gamma. The kinetics of expression is very transient for c-fos, reaching a maximum at 30 min and decreasing rapidly thereafter. The c-jun remained high throughout the stages analysed. Cycloheximide superinduced c-fos and c-jun induction by IFN-gamma, thus indicating that both act as immediate early genes. The products of c-fos and c-jun, proteins FOS and JUN, that act in conjunction forming the regulatory factor AP-1, were detected 1 hr after stimulation in virtually all cells, using flow cytometry. The induction in astrocytes of both proto-oncogenes could be the first stage of immunological activation of these central nervous system cells by immune interferon. 相似文献