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Effect of epidermal growth factor on the migration of neural stem cells

Neural Regeneration Research 2006年第6期1卷 502-504页

作者： Faliang Duan Guoping Yang Junwu Wei Jinglei Wu Department of Neurosurgery First Hospital of Wuhan Wuhan 430022 Hubei Province China

BACKGROUND： Recently, researches on neural stem cells （NSCs） are focus on differentiation and migration ot stem cells. How to regulate and control differentiation and migration of NSCs based on human wills is still a hot topic. OBJECTIVE ： To investigate the effect of epidermal growth factor （EGF） on the migration and proliferation of NSCs and analyze duration of the effect. DESIGN ： Contrast study based on cells SETTING ： Department of Neurological Surgery, the First Hospital of Wuhan MATERIALS： Healthy SD rats aged 13-14 embryonic days. EGF （Sigma Company） METHODS： The experiment was carried out in the Animal Laboratory of Experimental Center Affiliated to the First Hospital of Wuhan from October 2004 to July 2006. NSCs selected from embryonic striatum of rats with 13-14 embryonic days were cultured; 7 days later, suspended neural sphere was used to make simple cell suspension and cultured once more. Then, DMEM-F12＋20 μg/L EGF was added into culture medium; 14 days later, the rats were divided into experimental group and control group. Rats in the experimental group were cultured with the same medium mentioned above; however, rats in the control group were cultured with only DMEM-F12. Migration of cells was observed under microscope every day. MAIN OUTCOME MEASURES： NSCs migration in both experimental group and control group RESULTS： Cell spheres in primary culture were NSCs. In addition, 14 days later, proliferation of stem cells were observed remarkably in EGF culture, and size of cell sphere was about that of 100 cells. In experimental group, proliferation of cell sphere was slow down on the 14^th culture day, and apophysis was erupted to neighbor cell sphere. Moreover, NSCs migrated from big cell sphere to small cell sphere during 14-17 culture days, and then, cell migration was disappeared at 17 days after culture. In control group, cell migration was not observed. CONCLUSION： EGF can induce proliferation and migration of NSCs during a special

关键词：表皮生长因子/药理学大鼠 Sprague-Dawley 干细胞/药物作用纹状体/细胞学细胞培养的细胞运动/药物作用大鼠动物女(雌)性妊娠

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Requirement of SHP2 binding to Grb2-associated binder-1 for mitogen-activated protein kinase activation in response to lysophosphatidic acid and epidermal growth factor

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第18期275卷 13842-13848页

作者： Cunnick, JM Dorsey, JF Munoz-Antonia, T Mei, L Wu, J H Lee Moffitt Canc Ctr & Res Inst Mol Oncol Program MRC 3057E Tampa FL 33612 USA Univ S Florida Dept Med Microbiol & Immunol Tampa FL 33612 USA Univ S Florida Dept Biochem & Mol Biol Tampa FL 33612 USA Univ Alabama Birmingham Dept Neurobiol Birmingham AL 35294 USA

Grb2-associated binder-1 (Gab1) is a multisite docking protein containing a pleckstrin homology (PH) domain, multiple potential tyrosine phosphorylation sites, and several proline-rich sequences. Gab1 becomes tyrosine-phosphorylated in cells stimulated with growth factors, cytokines, and ligands for G protein-coupled receptors, A major Gab1-binding protein detected in cells treated with extracellular stimuli is the tyrosine phosphatase, SHP2. Although the role of SHP2-Gab1 interaction in cell signaling has not yet been characterized, SHP2 is known to mediate mitogen-activated protein (MAP) kinase activation induced by the epidermal growth factor (EGF), However, the mechanism by which the SHP2 phosphatase exerts a positive signaling role remains obscure. In this study, we prepared Gab1 mutants lacking the SHP2 binding site (Gab1Y627F), the phosphatidylinositol 3-kinase (PI3K) binding sites (Gab1 Delta PI3K), and the PH domain (Gab1 Delta PH). Expression of Gab1Y627F blocked the extracellular signal-regulated kinase-2 (ERK2) activation by lysophosphatidic acid (LPA) and EGF, Conversely, expression of the wild-type Gab1 in HEK293 cells augmented the LPA receptor Edg2-mediated ERK2 activation. Whereas the PH domain was required for Gab1 mediation of ERR2 activation by LPA, it was not essential for EGF-induced ERK2 activation. Expression of Gab1 Delta PI3K had no apparent effect on ERK2 activation by LPA and EGF in the cells that we have examined. These results establish a role for Gab1 in the LPA-induced MAP kinase pathway and clearly demonstrate that Gab1-SHP2 interaction is essential for ERK2 activation by LPA and EGF. These findings also suggest that the positive role of SHP2 in the MAP kinase pathway depends on its interaction with Gab1.

关键词： COS细胞酶激活表皮生长因子/代谢表皮生长因子/药理学细胞内信号肽和蛋白质类溶血磷脂素类/代谢溶血磷脂素类/药理学丝裂原激活蛋白激酶类/代谢磷蛋白类/代谢蛋白质结合蛋白质酪氨酸磷酸酶非受体11型蛋白酪氨酸磷酸酶非受体6型蛋白质酪氨酸磷酸酶类/代谢信号传导/药物作用动物

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Synergistic coupling of histone H3 phosphorylation and acetylation in response to epidermal growth factor stimulation

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MOLECULAR CELL 2000年第6期5卷 905-915页

作者： Cheung, P Tanner, KG Cheung, WL Sassone-Corsi, P Denu, JM Allis, CD Univ Virginia Dept Biochem & Mol Genet Charlottesville VA 22908 USA Oregon Hlth & Sci Univ Dept Biochem & Mol Biol Portland OR 97201 USA ULP INSERM CNRS Inst Genet & Biol Mol & Cellulaire F-67404 Illkirch Graffenstaden France

Histone acetylation and phosphorylation have separately been suggested to affect chromatin structure and gene expression. Here we report that these two modifications are synergistic. Stimulation of mammalian cells by epidermal growth factor (EGF) results in rapid and sequential phosphorylation and acetylation of H3, and these dimodified H3 molecules are preferentially associated with the EGF-activated c-fos promoter in a MAP kinase-dependent manner. In addition, the prototypical histone acetyltransferase Gcn5 displays an up to 10-fold preference for phosphorylated (Ser-10) H3 over nonphosphorylated H3 as substrate in vitro, suggesting that H3 phosphorylation can affect the efficiency of subsequent acetylation reactions. Together, these results illustrate how the addition of multiple histone modifications may be coupled during the process of gene expression.

关键词：乙酰化作用/药物作用乙酰基转移酶类/化学乙酰基转移酶类/遗传学乙酰基转移酶类/代谢氨基酸序列抗体/免疫学细胞系染色质/遗传学染色质/代谢 DNA结合蛋白质类表皮生长因子/药理学真菌蛋白质类/化学真菌蛋白质类/遗传学真菌蛋白质类/代谢基因表达调控/药物作用基因 fos/遗传学组蛋白酰基转移酶组蛋白类/化学组蛋白类/免疫学组蛋白类/代谢动力学 MAP激酶信号系统/药物作用小鼠近交C3H 丝裂原激活蛋白激酶类/代谢分子序列数据磷酰化/药物作用启动区遗传/遗传学蛋白激酶类/化学蛋白激酶类/遗传学蛋白激酶类/代谢酿酒酵母蛋白质类底物特异性动物小鼠

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Thyrotropin-releasing hormone and epidermal growth factor regulate iron-regulatory protein binding in pituitary cells via protein kinase C-dependent and -independent signaling pathways

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第41期275卷 31609-31615页

作者： Thomson, AM Rogers, JT Leedman, PJ Univ Western Australia Royal Perth Hosp Western Australian Inst Med Res Dept Med Perth WA 6000 Australia Univ Western Australia Royal Perth Hosp Western Australian Inst Med Res Lab Canc Med Perth WA 6000 Australia Harvard Univ Sch Med Massachusetts Gen Hosp E Genet & Aging Unit Charlestown MA 02129 USA

Intracellular iron homeostasis is regulated, in part, by interactions between iron-regulatory proteins (IRP1 and IRP2) and iron-responsive elements (IREs) in ferritin and transferrin receptor mRNAs. In addition to iron, cellular oxidative stress induced by H2O2, nitric oxide, and hypoxia, and hormonal activation by thyroid hormone and erythropoeitin have each been shown to regulate IRP binding to IREs. Hormonal signals, in particular mediated through protein kinase C (PKC), play a central role in the modulation of IRP/IRE interactions since phorbol esters were shown to activate IRP binding (Eisenstein, R. S., Tuazon, P. T., Schalinske, K. L., Anderson, S. A., and Traugh, J. A. (1993) J. Biol. Chem. 268, 27363-27370). In pituitary thyrotrophs (TtT97), we found that thyrotropin releasing hormone (TRH) and epidermal growth factor (EGF) increased IRP binding to a ferritin IRE, dependent on PKC and mitogen-activated protein kinase (MAPK) activity. In contrast, TRH and EGF decreased IRP binding in pituitary lactotrophs (GH3), despite activation of PKC and MAPK. IRP1 and IRP2 levels remained constant and IRP2 binding was predominant throughout. TRH and EGF markedly decreased IRP binding in MAPK kinase inhibitor-treated GH3 cells, whereas, they increased IRP binding in phosphatase inhibitor-treated GH3 cells. IRE-dependent CAT reporter translational expression closely reflected IRP binding to the ferritin IRE in both GH3 and TtT97 cells. Interestingly, ferritin protein levels were regulated similarly by TRH in both cell lines. These data link two different cell receptor systems to common signaling pathways that regulate IRP binding and ferritin expression. Remarkably, for TRH and EGF, these effects may be PKC-dependent or -independent determined by the cell type.

关键词：表皮生长因子/药理学铁蛋白质类/遗传学基因报告内环境稳定/药物作用铁/代谢铁调节蛋白质1 铁调节蛋白质2 铁调节蛋白质类铁硫蛋白质类/代谢 MAP激酶信号系统/药物作用丝裂原激活蛋白激酶类/拮抗剂和抑制剂丝裂原激活蛋白激酶类/代谢垂体/细胞学垂体/药物作用垂体/酶学垂体/代谢蛋白质结合/药物作用蛋白激酶C/拮抗剂和抑制剂蛋白激酶C/代谢 RNA/遗传学 RNA/代谢 RNA结合蛋白质类/代谢反应元件/遗传学信号传导/药物作用十四酰佛波乙酯/药理学促甲状腺素释放激素/药理学肿瘤细胞培养的增量调节/药物作用增量调节/遗传学动物大鼠

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Altered sensitivity to single-strand-specific reagents associated with the genomic vascular smooth muscle α-actin promoter during myofibroblast differentiation

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第20期275卷 15384-15391页

作者： Becker, NA Kelm, RJ Vrana, JA Getz, MJ Maher, LJ Mayo Clin & Mayo Fdn Dept Biochem & Mol Biol Rochester MN 55905 USA

Stimulation of quiescent AKR-2B mouse fibroblasts with transforming growth factor beta 1 results in uniform conversion to a myofibroblast-like phenotype as judged by a rapid accumulation of smooth muscle alpha-actin mRNA and protein. Because transcriptional regulation of the smooth muscle alpha-actin gene in these cells might be mediated by single-stranded DNA-binding proteins, we have examined the sensitivity of genomic DNA to chemical reagents with specificity for unpaired bases in a region of the promoter previously implicated in Pur alpha, Pur beta, and MSY1 binding in vitro (Kelm, R. J., Jr., Cogan, J. G., Elder, P. K., Strauch, A. R., and Getz, M. J. (1999) J, Biol. Chem. 274, 14238-14245), Our data reveal specific differences between purified DNA treated in vitro and nucleoprotein complexes treated in living cells. Although some differences were observed in quiescent cells, treatment with transforming growth factor beta 1 resulted in the development of additional sensitivity within 1 h. This enhancement was most pronounced in bases immediately upstream of an MCAT enhancer element-containing polypurine-polypyrimidine tract. A TATA-proximal element of similar base distribution showed no such hyperreactivities, These results suggest that activation of the endogenous smooth muscle alpha-actin gene during myofibroblast conversion is accompanied by specific structural changes in the promoter that are consistent with a decline in single-stranded DNA repressor protein binding.

关键词：肌动蛋白类/遗传学碱基序列细胞分化/药物作用 DNA 单链/药物作用增强子元件(遗传学) 表皮生长因子/药理学成纤维细胞/细胞学成纤维细胞/药物作用成纤维细胞/代谢胰岛素/药理学动力学分子序列数据肌平滑血管/代谢血小板源性生长因子/药理学启动区(遗传学) TATA盒转化生长因子β/药理学动物小鼠

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Epidermal growth factor protects epithelial cells against Fas-induced apoptosis - Requirement for Akt activation

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第25期274卷 17612-17618页

作者： Gibson, S Tu, S Oyer, R Anderson, SM Johnson, GL Univ Colorado Sch Med Program Mol Signal Transduct Div Basic SciNatl Jewish Med & Res Ctr Denver CO 80206 USA Univ Colorado Sch Med Dept Pathol Denver CO 80206 USA Univ Colorado Sch Med Dept Pharmacol Denver CO 80206 USA

Chemotherapeutic drugs that damage DNA kill tumor cells, in part, by inducing the expression of a death receptor such as Fas or its ligand, FastL. Here, we demonstrate that epidermal growth factor (EGF) stimulation of T47D breast adenocarcinoma and embryonic kidney epithelial (HEK293) cells protects these cells from Fas-induced apoptosis. EGF stimulation of epithelial cells also inhibited Fas-induced caspase activation and the proteolysis of signaling proteins downstream of the EGF receptor, Cbl and Akt/protein kinase B (Akt), EGF stimulation of Akt kinase activity blocked Fas-induced apoptosis. Expression of activated Akt in MCF-7 breast adenocarcinoma cells was sufficient to block Fas-mediated apoptosis, Inhibition of EGF-stimulated extracellular signal-regulated kinase (ERK) activity did not affect EGF protection from Fas-mediated apoptosis. The findings indicate that EGF receptor stimulation of epithelial cells has a significant survival function against death receptor-induced apoptosis mediated by Akt.

关键词：雄二烯类/药理学细胞凋亡钙-钙调素依赖性蛋白激酶类/代谢半胱氨酸天冬氨酸蛋白酶/代谢细胞系酶激活表皮生长因子/药理学上皮细胞/药物作用上皮细胞/生理学类黄酮物质/药理学蛋白质丝氨酸苏氨酸激酶原癌基因蛋白质类/代谢原癌基因蛋白质c-akt 人类

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ErbB receptor-induced activation of Stat transcription factors is mediated by Src tyrosine kinases

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第24期274卷 17209-17218页

作者： Olayioye, MA Beuvink, I Horsch, K Daly, JM Hynes, NE Friedrich Miescher Inst CH-4002 Basel Switzerland

Epidermal growth factor (EGF) binding to its receptor, ErbB1, triggers various signal transduction pathways, one of which leads to the activation of signal transducer and activator of transcription (Stat) factors. The mechanism underlying ErbB1-induced Stat activation and whether Stats are downstream targets of other ErbB receptors have not been explored. In this report we show that ErbB2, ErbB3, and ErbB4 do not potentiate Stat5 phosphorylation by EGF, However, neu differentiation factor-induced heterodimers of ErbB2 and ErbB4 activated Stat5. In A431 cells, Stat1, Stat3, and Stat5, were constitutively complexed with ErbB1 and rapidly phosphorylated on tyrosine in response to EGF. Neither mutation of the conserved tyrosine residue (Tyr(694)) nor inactivation of the Stat5a SH2 domain disrupted this association. However, an intact SH2 domain was necessary for EGF-induced Stat5a phosphorylation, In contrast to prolactin, which induced only Tyr(694) phosphorylation of Stat5a, EGF promoted phosphorylation on Tyr(694) and additional tyrosine residue(s). Janus kinases (Jaks) were also constitutively associated with ErbB receptors and were phosphorylated in response to EGF-related ligands, However, we provide evidence that EGF- and neu differentiation factor-induced Stat activation are dependent on Src but not Jak kinases. Upon EGF stimulation, c-Src was rapidly recruited to Stat/ ErbB receptor complexes. Pharmacological Src kinase inhibitors and a dominant negative c-Src ablated both Stat and Jak tyrosine phosphorylation, However, dominant negative Jaks did not affect EGF-induced Stat phosphorylation, Taken together, the experiments establish two independent roles for Src kinases: (i) key molecules in ErbB receptor-mediated Stat signaling and (ii) potential upstream regulators of Jak kinases.

关键词：表皮生长因子/药理学模型生物学磷酰化催乳素/药理学原癌基因蛋白质类/代谢受体 erbB-2/代谢受体 erbB-3 受体细胞表面/代谢信号传导反式激活因子类/代谢 src族激酶类/代谢

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Control sites of ribosomal S6 kinase B and persistent activation through tumor necrosis factor

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第31期275卷 23549-23558页

作者： Tomás-Zuber, M Mary, JL Lesslauer, W Yale Univ Sch Med Dept Epidemiol & Publ Hlth New Haven CT 06520 USA Yale Univ Sch Med Immunobiol Sect New Haven CT 06520 USA F Hoffmann La Roche & Co Ltd Dept PRPN CH-4070 Basel Switzerland F Hoffmann La Roche & Co Ltd Dept PRPV CH-4070 Basel Switzerland

RSKB, a 90-kDa ribosomal S6 protein kinase family (RSK) member with two complete catalytic domains connected by a linker, is activated through p38- and ERK-mitogen-activated protein kinases, The N-terminal kinases of RSKs phosphorylate substrates;activation requires phosphorylation of linker and C-terminal kinase sites. Unlike other RSKs, the activation loop phosphorylation sites of both catalytic domains of RSKB, Ser(196) and Thr(568), were required for activity. RSKB activation depended on phosphorylation of linker Ser(343) and Ser(360) and associated with phosphorylation of nonconserved Ser(347), but Ser(347)-deficient RSKB retained partial activity. The known protein kinase A and protein kinase C inhibitors, H89 and Ro31-8220, blocked RSKB activity. Treatment of HeLa cells with tumor necrosis factor, epidermal growth factor, phorbol 12-myristate 13-acetate, and ionomycin but not: with insulin resulted in strong activation of endogenous RSKB, High RSKB activity and Ser(347)/Ser(360) phosphorylation persisted for 3 h in tumor necrosis factor-treated cells, in contrast to the short bursts of p38, ERK, and RSK1-3 activities. In conclusion, a variety of stimuli induced phosphorylation and activation of RSKB through both p38 and ERK pathways;the persistence of activation indicated that RSKB selectively escaped cell mechanisms causing rapid deactivation of upstream p38 and ERK and other RSKs.

关键词：氨基酸序列催化域环AMP依赖性蛋白激酶类/拮抗剂和抑制剂酶激活酶抑制剂/药理学表皮生长因子/药理学 HeLa细胞吲哚类/药理学胰岛素/药理学离子霉素/药理学异喹啉类/药理学丝裂原激活蛋白激酶类/代谢分子序列数据磷酰化蛋白质结合蛋白激酶C/拮抗剂和抑制剂蛋白质结构三级重组蛋白质类/代谢核糖体蛋白质S6激酶类/拮抗剂和抑制剂核糖体蛋白质S6激酶类/遗传学核糖体蛋白质S6激酶类/代谢丝氨酸信号传导底物特异性磺胺类十四酰佛波乙酯/药理学苏氨酸肿瘤坏死因子α/药理学人类

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Activation of epidermal growth factor receptor promotes late terminal differentiation of cell-matrix interaction-disrupted keratinocytes

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第52期274卷 37285-37291页

作者： Wakita, N Takigawa, M Hamamatsu Univ Sch Med Dept Dermatol Hamamatsu Shizuoka 4313192 Japan

The biological effects of epidermal growth factor receptor (EGFR) activation may differ between epidermal suprabasal and basal keratinocytes, since growth factors are mitogenic in adherent cells only in the presence of cell-extracellular matrix (ECM) interaction, To investigate biological effects of EGFR activation on keratinocytes without cell-ECM interaction, we cultured normal human keratinocytes on polyhydroxyethyl-methacrylate-coated plates, which disrupt cell-ECM but not cell-cell interaction. The cells initially expressed keratin 10 (K10) and then profilaggrin, mimicking sequential differentiation of epidermal suprabasal keratinocytes, The addition of EGF or transforming growth factor-alpha promoted late terminal differentiation (profilaggrin expression, type 1 transglutaminase expression and activity, and cornified envelope formation) of the suspended keratinocytes, while suppressing K10 expression, an early: differentiation marker. These effects were attenuated by EGFR tyrosine kinase inhibitor PD153035 or an anti-EGFR monoclonal antibody, whereas protein kinase C inhibitors H7 and bisindolylmaleimide I or mitogen-activated protein kinase/extracellular signal-regulated kinase kinase inhibitor PD98059 abolished profilaggrin up-regulation but not K10 suppression. Since the antidifferentiative role of EGFR on cell-ECM interaction-conserved keratinocytes has been well documented, our results indicate that the biological effects of EGFR:on keratinocytes are influenced by cell-ECM interaction and suggest that EGFR activation promotes rather than inhibits the terminal differentiation of suprabasal epidermal keratinocytes.

关键词： 1-(5-异喹啉磺酰基)-2-甲基哌嗪/药理学细胞分化/药物作用细胞培养的酶激活表皮生长因子/药理学细胞外基质/生理学类黄酮物质/药理学中间丝蛋白质类/生物合成角蛋白细胞/生理学角蛋白质类/生物合成蛋白激酶C/生理学蛋白质前体/生物合成转谷酰胺酶/生物合成动物人类小鼠

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Growth and antrum formation of bovine preantral follicles in long-term culture in vitro

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BIOLOGY OF REPRODUCTION 2000年第5期62卷 1322-1328页

作者： Gutierrez, CG Ralph, JH Telfer, EE Wilmut, I Webb, R Roslin Inst Roslin EH25 9PS Midlothian Scotland Univ Edinburgh Sch Agr Bldg Div Biol Sci IERM Edinburgh EH9 3JG Midlothian Scotland Univ Nottingham Sch Biol Sci Div Agr & Hort Loughborough LE12 5RD Leics England

Culture of preantral follicles has important biotechnological implications through its potential to produce large quantities of oocytes for embryo production and transfer. A long-term culture system for bovine preantral follicles is described. Bovine preantral follicles (166 +/- 2.15 pm), surrounded by theta cells, were isolated from ovarian cortical slices. Follicles were cultured under conditions known to maintain granulosa cell viability in vitro. The effects of epidermal growth factor (EGF), insulin-like growth factor (IGF)-I, FSH, and coculture with bovine granulosa cells on preantral follicle growth were analyzed. Follicle and oocyte diameter increased significantly (P < 0.05) with time in culture. FSH, IGF-I, and EGF stimulated (P < 0.05) follicle growth rate but had no effect on oocyte growth. Coculture with granulosa cells inhibited FSH/ICF-I-stimulated growth. Most follicles maintained their morphology throughout culture, with the presence of a thecal layer and basement membrane surrounding the granulosa cells. Antrum formation, confirmed by confocal microscopy, occurred between Days 10 and 28 of culture. The probability of follicles reaching antrum development was 0.19 for control follicles. The addition of growth factors or FSH increased (P < 0.05) the probability of antrum development to 0.55. Follicular growth appeared to be halted by slower growth of the basement membrane, as growing follicles occasionally burst the basement membrane, extruding their granulosa cells. In conclusion, a preantral follicle culture system in which follicle morphology can be maintained for up to 28 days has been developed. In this system, FSH, EGF, and IGF-I stimulated follicle growth and enhanced antrum formation. This culture system may provide a valuable approach for studying the regulation of early follicular development and for production of oocytes for nuclear/embryo transfer, but further work is required.

关键词：细胞培养技术/方法细胞分裂/药物作用细胞培养的表皮生长因子/药理学卵泡刺激素/药理学胰岛素样生长因子Ⅰ/药理学卵泡/细胞学卵泡/药物作用卵泡/生理学动物牛女(雌)性

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