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Integrin-mediated muscle cell spreading - The role of protein kinase C in outside-in and inside-out signaling and evidence of integrin cross-talk

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第45期274卷 32486-32492页

作者： Disatnik, MH Rando, TA Stanford Univ Med Ctr Dept Neurol & Neurol Sci Sch Med Stanford CA 94305 USA Vet Affairs Med Ctr Dept Neurol & Neurol Sci Stanford CA 94305 USA

Muscle cell survival depends upon the presence of various integrins with affinities for different extracellular matrix proteins. The absence of either alpha(5) or alpha(7) integrins leads to degenerative disorders of skeletal muscle, muscular dystrophies. To understand the cell survival signals that are mediated by integrin engagement with matrix proteins, we studied the early signaling events initiated by the attachment of muscle cells to fibronectin, an interaction that is mediated primarily by alpha(5) integrins, Cells that express alpha(5) integrin rapidly spread on fibronectin, and this process is associated with the phosphorylation of focal adhesion kinase (FAK). Cells deficient in alpha(5) integrin failed to spread or promote FAK phosphorylation when plated on fibronectin, For alpha(5)-expressing cells, both spreading and FAK phosphorylation could be blocked by inhibitors of protein kinase C (PKC), indicating that PKC is necessary for this "outside-in signaling" mediated by alpha(5) integrin. Surprisingly, activators of PKC could promote spreading and FAK phosphorylation in alpha(5)-deficient muscle cells plated on fibronectin, This PKC-induced cell spreading appeared to be due to activation of alpha(4) integrins ("inside-out signaling") since it could be blocked by peptides that specifically inhibit alpha(4) integrin binding to fibronectin, A model of integrin signaling in muscle cells is presented in which there is a positive feedback loop involving PHC in both outside-in and inside-out signaling, and the activation of this cycle is essential for cell spreading and downstream signaling to promote cell survival. In addition, the data indicate a cross-talk that occurs between integrins in which the outside-in signaling via one integrin can promote the activation of another integrin via inside-out signaling.

关键词：细胞运动/生理学细胞存活细胞培养的整合素类/生理学模型生物学肌/生理学蛋白激酶C/代谢受体纤连蛋白/生理学信号传导动物小鼠

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Platelet-derived growth factor receptor β regulates migration and DNA synthesis in metanephric mesenchymal cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第13期275卷 9527-9533页

作者： Arar, M Xu, YC Elshihabi, I Barnes, JL Choudhury, GG Abboud, HE Univ Texas Hlth Sci Ctr Dept Pediat San Antonio TX 78229 USA Univ Texas Hlth Sci Ctr Dept Internal Med San Antonio TX 78229 USA S Texas Dept Vet Affairs Hlth Care Syst Ctr Geriatr Res Educ & Clin San Antonio TX 78229 USA

Platelet-derived growth factor (PDGF) B-chain and PDGF receptor beta (PDGFR beta) are essential for glomerulogenesis, Mice deficient in PDGF B-chain or PDGFR beta exhibit an abnormal glomerular phenotype characterized by total lack of mesangial cells. In this study, we localized PDGFR beta in the developing rat kidney and explored the biological effects of PDGF in metanephric mesenchymal cells in an attempt to determine the mechanism by which PDGF regulates mesangial cell development. Immunohistochemical and in situ hybridization studies of rat embryonic kidneys reveal that PDGFR beta localizes to undifferentiated metanephric mesenchyme and is later expressed in the cleft of the comma-shaped and S-shaped bodies and in more mature glomeruli in a mesangial distribution. We also isolated and characterized cells from rat metanephric mesenchyme. Metanephric mesenchymal cells express vimentin and alpha-smooth muscle actin but not cytokeratin, These cells also express functional PDGFR beta, as demonstrated by autophosphorylation of the receptor as well as activation of phosphatidylinositol 3 kinase in response to PDGF B-chain homodimer, PDGF B-chain also induces migration and proliferation of metanephric mesenchymal cells. Taken together with the fact that PDGF B-chain is expressed in the glomerular epithelium and mesangial area, as demonstrated in the human embryonic kidney, we suggest that PDGF B-chain acts in a paracrine fashion to stimulate the migration and proliferation of mesangial cell precursors from undifferentiated metanephric mesenchyme to the mesangial area. PDGF B-chain also likely stimulates proliferation of mesangial cell precursors in an autocrine fashion once these cells migrate to the glomerular tuft.

关键词：细胞运动/生理学细胞培养的 DNA复制/生理学上皮细胞/细胞学上皮细胞/代谢免疫组织化学肾/细胞学肾/胚胎学肾/代谢蛋白质结合大鼠 Sprague-Dawley 受体血小板源生长因子β/代谢受体血小板源生长因子β/生理学动物小鼠大鼠

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Chondrocyte translocation response to direct current electric fields

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JOURNAL OF BIOMECHANICAL ENGINEERING-TRANSACTIONS OF THE ASME 2000年第3期122卷 261-267页

作者： Chao, PHG Roy, R Mauck, RL Liu, W Valhmu, WB Hung, CT Columbia Univ Dept Biomed Engn Cellular Engn Lab New York NY 10027 USA Columbia Univ Dept Orthopaed Surg Orthopaed Res Lab New York NY 10032 USA

Using a custom galvanotaxis chamber and time-lapse digital video microscopy, we report the novel observation that cultured chondrocytes exhibit cathodal migration when subjected to applied direct current (DC) electric fields as low as 0.8 V/cm. The response was dose-dependent for field strengths greater than 4 V/cm. Cell migration appeared to be an active process with extension of cytoplasmic processes in the direction of movement. In some cells, field application for greater than an hour induced elongation of initially round cells accompanied by perpendicular alignment of the long axis with respect to the applied field. Antagonists of the inositol phospholipid pathway, U-73122 and neomycin, were able to inhibit cathodal migration. Cell migration toward the cathode did nor require the presence of serum during field application. However, the directed velocity was nearly threefold greater in studies performed with serum. Studies performed at physiologic temperatures (similar to 37 degreesC) revealed a twofold enhancement in migration speed compared to similar studies at room temperature (similar to 25 degreesC). Findings from the present study may help to elucidate basic mechanisms that mediate chondrocyte migration and substrate attachment. Since chondrocyte migration has been implicated in cartilage healing, the ability to direct chondrocyte movement has the potential to impact strategies for addressing cartilage healing/repair and for development of cartilage substitutes.

关键词：细胞运动/药物作用细胞运动/生理学细胞培养的/药物作用细胞培养的/生理学软骨细胞/药物作用软骨细胞/生理学电刺激雌烯类显微镜检查电视新霉素/药理学磷酸二酯酶抑制剂/药理学吡咯烷酮类动物牛

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Analysis of biological effects and signaling properties of Flt-1 (VEGFR-1) and KDR (VEGFR-2) - A reassessment using novel receptor-specific vascular endothelial growth factor mutants

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JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第5期276卷 3222-3230页

作者： Gille, H Kowalski, J Li, B LeCouter, J Moffat, B Zioncheck, TF Pelletier, N Ferrara, N Genentech Inc Dept Mol Oncol San Francisco CA 94080 USA Genentech Inc Dept Prot Engn San Francisco CA 94080 USA Genentech Inc Dept Metab & Pharmacokinet San Francisco CA 94080 USA Genentech Inc Dept Prot Chem San Francisco CA 94080 USA

Endothelial cells express two related vascular endothelial growth factor (VEGF) receptor tyrosine kinases, KDR (kinase-insert domain containing receptor, or VEGFR-2) and Flt-1 (fms-like tyrosine kinase, or VEGFR-1). Although considerable experimental evidence links KDR activation to endothelial cell mitogenesis, there is still significant uncertainty concerning the role of individual VEGF receptors for other biological effects such as vascular permeability, VEGF mutants that bind to either KDR or Fit-1 with high selectivity were used to determine which of the two receptors serves to mediate different VEGF functions. In addition to mediating mitogenic signaling, selective KDR activation was sufficient for the activation of intracellular signaling pathways implicated in cell migration. KDR stimulation caused tyrosine phosphorylation of both phosphatidylinositol 3-kinase and phospholipase C gamma in primary endothelial cells and stimulated cell migration. KDR-selective VEGF was also able to induce angiogenesis in the rat cornea to an extent indistinguishable from wild type VEGF, We also demonstrate that KDR, but not Flt-1, stimulation is responsible for the induction of vascular permeability by VEGF.

关键词： 1-磷脂酰肌醇3-激酶/代谢毛细血管通透性/生理学细胞运动/生理学细胞培养的内皮生长因子/代谢内皮血管/细胞学内皮血管/生理学酶激活同工酶类/代谢淋巴因子/代谢丝裂原激活蛋白激酶类/代谢突变新生血管化生理性/生理学磷脂酶Cγ 原癌基因蛋白质类/生理学受体蛋白质酪氨酸激酶类/生理学受体生长因子/生理学受体血管内皮生长因子信号传导/生理学血管内皮生长因子A 血管内皮生长因子受体1 血管内皮生长因子类人类

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Vascular endothelial growth factor (VEGF)-driven actin-based motility is mediated by VEGFR2 and requires concerted activation of stress-activated protein kinase 2 (SAPK2/p38) and geldanamycin-sensitive phosphorylation of focal adhesion kinase

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第14期275卷 10661-10672页

作者： Rousseau, S Houle, F Kotanides, H Witte, L Waltenberger, J Landry, J Huot, J Univ Laval Hotel Dieu Quebec Ctr Rech Cancerol Quebec City PQ G1R 2J6 Canada Univ Ulm Med Ctr Dept Internal Med 2 D-89081 Ulm Germany ImClone Syst Inc Dept Mol & Cell Biol New York NY 10014 USA

In endothelial cells, vascular endothelial growth factor (VEGF) induces an accumulation of stress fibers associated with new actin polymerization and rapid formation of focal adhesions at the ventral surface of the cells. This cytoskeletal reorganization results in an intense motogenic activity. Using porcine endothelial cells expressing one or the other type of the VEGF receptors, VEGFR1 or VEGFR2, or human umbilical vein endothelial cells pretreated with a VEGFR2 neutralizing antibody, we show that VEGFR2 is responsible for VEGF-induced activation of the stress-activated protein kinase-2/p38 (SAPK2/p38), phosphorylation of focal adhesion kinase (FAK), and enhanced migratory activity. Activation of SAPK2/p38 triggered actin polymerization whereas FAX, which was phosphorylated independently of SAPK2/p38, initiated assembly of focal adhesions. Both processes contributed to the formation of stress fibers. Geldanamycin, an inhibitor of HSP90 blocked tyrosine phosphorylation of FAK, assembly of focal adhesions, actin reorganization, and cell, migration, all of which were reversed by overexpressing HSP90. We conclude that VEGFR2 mediates the physiological effect of VEGF on cell migration and that two independent pathways downstream of VEGFR2 regulate actin-based motility. One pathway involves SAPK2/p38 and leads to enhanced actin polymerization activity. The other involves HSP90 as a permissive signal transduction factor implicated in FAK phosphorylation and assembly of focal adhesions.

关键词：肌动蛋白类/生理学抗体/药理学苯醌类钙-钙调素依赖性蛋白激酶类/代谢细胞黏附细胞运动/药物作用细胞运动/生理学细胞培养的细胞支架蛋白质类/生理学内皮生长因子/药理学内皮血管/细胞学内皮血管/药物作用内皮血管/生理学酶激活黏着斑激酶1 黏着斑蛋白酪氨酸激酶类 HSP90热休克蛋白质类/拮抗剂和抑制剂 HSP90热休克蛋白质类/遗传学 HSP90热休克蛋白质类/生理学内酰胺类大环淋巴因子/药理学丝裂原激活蛋白激酶类桩蛋白磷蛋白类/生理学磷酰化蛋白酪氨酸激酶类/拮抗剂和抑制剂蛋白酪氨酸激酶类/代谢原癌基因蛋白质类/生理学醌类/药理学受体蛋白质酪氨酸激酶类/免疫学受体蛋白质酪氨酸激酶类/生理学受体生长因子/免疫学受体生长因子/生理学受体血管内皮生长因子脐静脉血管内皮生长因子A 血管内皮生长因子受体1 血管内皮生长因子类纽蛋白/生理学 p38丝裂原活化蛋白激酶类人类

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The very low density lipoprotein receptor regulates urokinase receptor catabolism and breast cancer cell motility in vitro

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第11期274卷 7412-7420页

作者： Webb, DJ Nguyen, DHD Sankovic, M Gonias, SL Univ Virginia Hlth Sci Ctr Dept Pathol Charlottesville VA 22908 USA Univ Virginia Hlth Sci Ctr Dept Biochem & Mol Genet Charlottesville VA 22908 USA

The very low density lipoprotein receptor (VLDLr) binds diverse ligands, including urokinase-type plasminogen activator (uPA) and uPA-plasminogen activator inhibitor-1 (PAI-1) complex. In this study, we characterized the effects of the VLDLr on the internalization, catabolism, and function of the uPA receptor (uPAR) in MCF-7 and MDA-MB-435 breast cancer cells. When challenged with uPA . PAI-1 complex, MDA-MB-435 cells internalized uPAR;this process was inhibited by 80% when the activity of the VLDLr was neutralized with receptor-associated protein (RAP), To determine whether internalized uPAR is degraded, we studied the catabolism of [S-35]methionine-labeled uPAR. In the absence of exogenous agents, the uPAR catabolism t(1/2) was 8.2 h. uPA . PAI-1 complex accelerated uPAR catabolism (t(1/2) to 1.8 h), while RAP inhibited uPAR catabolism in the presence (t(1/2) of 7.8 h) and absence (t(1/2) of 16.9 h) of uPA . PAI-1 complex, demonstrating a critical role for the VLDLr, When MCF-7 cells were cultured in RAP, cell surface uPAR levels increased gradually, reaching a new steady-state in 3 days, The amount of uPA which accumulated in the medium also increased. Culturing in RAP for 3 days increased MCF-7 cell motility by 2.2 +/- 0.1-fold and by 4.4 +/- 0.3-fold when 1.0 nm uPA was added. The effects of RAP on MCF-7 cell motility were entirely abrogated by an antibody which binds uPA and prevents uPA binding to uPAR. MCF-7 cells that were cultured in RAP demonstrated increased levels of activated mitogen-activated protein kinases, Furthermore, the MEK inhibitor, PD098059, decreased the motility of RAP-treated cells without affecting control cultures. These studies suggest a model in which the VLDLr regulates autocrine uPAR-initiated signaling and thereby regulates cellular motility.

关键词：乳腺肿瘤/酶学乳腺肿瘤/代谢乳腺肿瘤/病理学钙-钙调素依赖性蛋白激酶类/代谢载体蛋白质类/代谢细胞运动/生理学胞吞作用酶激活谷胱甘肽转移酶/代谢水解作用脂蛋白类 VLDL/代谢受体细胞表面/代谢受体 LDL/代谢受体 LDL/生理学受体尿激酶型纤溶酶原激活物重组融合蛋白质类/代谢肿瘤细胞培养的人类

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Multimeric structure of PomA, a component of the Na⁺-driven polar flagellar motor of Vibrio alginolyticus

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第26期275卷 20223-20228页

作者： Sato, K Homma, M Nagoya Univ Grad Sch Sci Div Biol Sci Chikusa Ku Nagoya Aichi 4648602 Japan

Four integral membrane proteins, PomA, PomB, MotX, and MotY, are thought to be directly involved in torque generation of the Na+-driven polar flagellar motor of Vibrio alginolyticus. Our previous study showed that PomA and PomB form a complex, which catalyzes sodium influx in response to a potassium diffusion potential. PomA forms a stable dimer when expressed in a PomB null mutant. To explore the possible functional dependence of PomA domains in adjacent subunits, we prepared a series of PomA dimer fusions containing different combinations of wild-type or mutant subunits, Introduction of the mutation P199L, which completely inactivates flagellar rotation, into either the first or the second half of the dimer abolished motility. The P199L mutation in monomeric PomA also altered the PomA-PomB interaction. PomA dimer with the P199L mutation even in one subunit also had no ability to interact with PomB, indicating that the both subunits in the dimer are required for the functional interaction between PomA and PomB, Flagellar rotation by wild-type PomA dimer was completely inactivated by phenamil, a sodium channel blocker. However, activity was retained in the presence of phenamil when either half of the dimer was replaced with a phenamil-resistant subunit, indicating that both subunits must bind phenamil for motility to be fully inhibited. These observations demonstrate that both halves of the PomA dimer function together to generate the torque for flagellar rotation.

关键词：阿米洛利/类似物和衍生物阿米洛利/药理学细菌蛋白质类细胞膜/化学细胞运动/生理学二聚作用剂量效应关系药物电泳聚丙烯酰氨凝胶鞭毛/化学突变蛋白质结构三级重组融合蛋白质类/化学钠/代谢钠通道/化学钠通道/遗传学氯化钠/药理学弧菌属/化学

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Engineered alignment in media equivalents: Magnetic prealignment and Mandrel compaction

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JOURNAL OF BIOMECHANICAL ENGINEERING-TRANSACTIONS OF THE ASME 1998年第5期120卷 660-666页

作者： Barocas, VH Girton, TS Tranquillo, RT Univ Minnesota Dept Chem Engn & Mat Sci Minneapolis MN 55455 USA Univ Minnesota Inst Biomed Engn Minneapolis MN 55455 USA

We predicted and measured the evolution of smooth muscle cell (SMC) orientation in media-equivalents (MEs) for four fabrication conditions (F-, M-, F+, M+) under Free or Mandrel compaction (F/M) with and without magnetic prealignment of the collagen fibrils in the circumferential direction (+/-). Mandrel compaction refers to SMC-induced compaction of the ME that is constrained by having a nonadhesive mandrel placed in the ME lumen. Predictions were made using our anisotropic biphasic theory (ABT) for tissue-equivalent mechanics. Successful prediction of trends of the SMC orientation data for all four fabrication cases was obtained: maintenance of the initial isotropic state for F-, loss of initial circumferential alignment for F+, development of circumferential alignment for M-, and enhancement of initial circumferential alignment for M+. These results suggest two mechanisms by which the presence of the mandrel leads to much greater mechanical stiffness in the circumferential direction reported for mandrel compacted MEs relative to free compacted MEs : (I) by inducing an increasing circumferential alignment of the SMC and collagen, and (2) by inducing a large sb ess on the SMC, resulting in secretion and accumulation of stiffening components.

关键词：各向异性细胞黏附细胞运动/生理学细胞极性/生理学胶原/生理学培养技术/方法弹性磁力学膜人工模型生物学肌平滑/细胞学试验预期值压力结果可重复性流变学动物牛大鼠

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CCN5 is a growth arrest-specific gene that regulates smooth muscle cell proliferation and motility

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AMERICAN JOURNAL OF PATHOLOGY 2003年第1期162卷 219-231页

作者： Lake, AC Bialik, A Walsh, K Castellot, JJ Tufts Univ Sch Med Dept Anat & Cell Biol Boston MA 02111 USA Boston Univ Sch Med Whitaker Cardiovasc Inst Boston MA 02118 USA Tufts Univ Sackler Sch Grad Biomed Sci Program Cell Mol & Dev Biol Boston MA 02111 USA

Vascular smooth muscle cell (VSMC) hyperplasia plays an important role in both chronic and acute vascular pathologies. Considerable work has focused on the mechanisms regulating VSMC growth and the search for agents that could suppress VSMC hyper-proliferation. One of the several inhibitors studied is the glycosaminoglycan heparin, which inhibits VSMC proliferation and migration both in cell culture and in animal models (Mishra-Gorur K, Delmolino LM, Castellot Jr JJ: Biological functions of heparan sulfate and heparan sulfate proteoglycans. Trends Glycosci Glycotechnol 1998, 10:193-210). To aid our understanding of the anti-proliferative mechanism of action of heparin, we used a subtractive hybridization approach to isolate and characterize a novel growth arrest-specific (gas) gene induced in VSMCs exposed to heparin (Delmolino LM, Stearns NA, Castellot Jr JJ: Heparin induces a member of the CCN family which has characteristics of a growth arrest specific gene. Mol Biol Cell 1997, 8:287a and Delmolino IM, Stearns NA, Castellot Jr JJ: COP-1, a member of the CCN family, is a heparin-induced growth arrest specific gene in vascular smooth muscle cells. J Cell Physiol 2001, 188:45-55). This gene is a member of the cysteine-rich 61/connective tissue growth factor/nephroblastoma-overexpressed (CCN) family and has been given the name CCN5. In this report, we provide functional evidence that CCN5 can inhibit VSMC proliferation, motility, and invasiveness. In contrast, adhesion and apoptosis are unaffected by CCN5 in this cell type. We also significantly extend previous data from our laboratory that suggests CCN5 is a growth arrest-specific (gas) gene. Furthermore, we map for the first time the cellular localization of CCN5 protein in cultured VSMCs. We also examine uninjured and balloon-injured rat carotid arteries for CCN5 expression. The results from the in vitro and in vivo localization studies show that CCN5 is temporally and spatially expressed in a manner consistent wi

关键词：腺病毒科/遗传学 CCN胞间信号蛋白质类颈动脉疾病/遗传学颈动脉疾病/代谢颈动脉疾病/病理学细胞黏附/生理学细胞分裂/生理学细胞迁移抑制细胞运动/生理学细胞培养的遗传载体/遗传学遗传载体/药理学肝素/药理学肌平滑血管/代谢肌平滑血管/病理学大鼠 Sprague-Dawley 阻遏蛋白质类/遗传学阻遏蛋白质类/代谢阻遏蛋白质类/药理学转染动物男(雄)性大鼠

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GABA receptor antagonists modulate postmitotic cell migration in slice cultures of embryonic rat cortex

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CEREBRAL CORTEX 2000年第9期10卷 899-909页

作者： Behar, TN Schaffner, AE Scott, CA Greene, CL Barker, JL NINDS Neurophysiol Lab NIH Bethesda MD 20892 USA

Recent studies indicate that GABA acts as a chemoattractant during rat cortical histogenesis. In vivo, GABA localizes in appropriate locations for a chemoattractant, along migratory routes and near target destinations for migrating cortical neurons. In vitro, GABA induces dissociated embryonic cortical neurons to migrate. Here, embryonic rat cortical slices were cultured in the presence or absence of GABA receptor (GABA-R) antagonists to assess GABA's Effects on neuronal migration in situ. Gestational day 18 (E18) cortical slices were incubated overnight in bromodeoxyuridine (BrdU)-containing medium to label ventricular zone (vz) cells as they underwent terminal mitosis. The slices were then cultured in BrdU-free medium with or without GABA-R antagonists. In control slices, most BrdU(+) cells were observed in the cortical plate (cp) after 48 h. in contrast, cultures maintained in either saclofen (a GABA(B)-R antagonist) or picrotoxin (a GABA(A/C)-R antagonist) had few BrdU-labeled cp cells. However, the effects of the two antagonists were distinct. In the picrotoxin-treated slices, nearly half of all BrdU(+) cells remained in the vz and subventricular zone (svz), whereas saclofen treatment resulted in an accumulation of BrdU(+) cells in the intermediate zone (iz). Bicuculline, a GABA(A)-R antagonist, did not block, but rather enhanced migration of BrdU(+) cells into the cp. These results provide evidence that picrotoxin-sensitive receptors promote the migration of vz/svz cells into the it, while saclofen sensitive receptors signal cells to migrate into the cp. Thus, as cortical cells differentiate, changing receptor expression appears to modulate migratory responses to GABA.

关键词：巴氯芬/类似物和衍生物巴氯芬/药理学荷包牡丹碱/药理学溴脱氧尿苷/分析细胞运动/药物作用细胞运动/生理学大脑皮质/细胞学大脑皮质/药物作用大脑皮质/胚胎学趋化作用/药物作用 GABA拮抗剂/药理学神经胶质原纤维酸性蛋白质/分析中间丝蛋白质类/分析有丝分裂神经组织蛋白质类神经胶质/细胞学神经元/化学神经元/细胞学神经元/生理学器官培养技术印防己毒素/药理学受体 GABA-A/生理学 γ氨基丁酸/药理学动物女(雌)性妊娠大鼠

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