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Human macrophage adhesion on fibronectin: The role of substratum and intracellular signalling kinases

机译:人巨噬细胞粘附在纤连蛋白上:基质和细胞内信号激酶的作用

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Fibronectin and Arg-Gly-Asp (RGD)- and/or Pro-His-Ser-Arg-Asn (PHSRN)-containing oligopeptides were immobilized onto physicochemically distinct substrata: polyethyleneglycol-based networks or tissue culture polystyrene (TCPS). The role of selected signalling kinases in the adhesion of human primary blood-derived macrophages on these modified Substrata was investigated. We demonstrated that the protein tyrosine kinase (PTK) or protein serine/threonine kinase (PSK) dependency and the PTK PSK cross-talk compensation For macrophage adhesion varied dynamically with the substratum modification and the culture time. The inhibition of MAPK kinase (MAPKK) decreased macrophage adhesion oil TCPS, whereas the inhibition of phosphoinositide-3 kinase (PI3 kinase) decreased macrophage adhesion oil networks at 24 h, The PI3 kinase-protein kinase C (PKC)-MAPK cascade was involved in macrophage adhesion on fibronectin-preadsorbed TCPS or networks but not oil fibronectin-grafted networks, This fibronectin-mediated adhesion signalling involved both RGD and PHSRN sequences in a form of G(3)RGDG(6)PHSRNG on TCPS but not oil networks. Furthermore, G(3)RGDG(6)PHSRNG grafted onto networks evoked unique signalling in macrophage adhesion From that preadsorbed onto networks. Thus, macrophage adhesion and the role of selected signalling kinases were modulated by the substratum and the ligand conjugation method. (C) 2002 Elsevier Science Inc. All rights reserved. [References: 30]
机译:将含有纤连蛋白和Arg-Gly-Asp(RGD)和/或Pro-His-Ser-Arg-Asn(PHSRN)的寡肽固定在物理化学上不同的基质上:基于聚乙二醇的网络或组织培养聚苯乙烯(TCPS)。研究了选定的信号激酶在人类原代血液巨噬细胞粘附于这些修饰的基质上的作用。我们证明蛋白质酪氨酸激酶(PTK)或蛋白质丝氨酸/苏氨酸激酶(PSK)依赖性和PTK PSK串扰补偿巨噬细胞粘附随基质修饰和培养时间而动态变化。 MAPK激酶(MAPKK)的抑制作用可降低巨噬细胞黏附油TCPS,而磷酸肌醇3激酶(PI3激酶)的抑制作用则可在24小时内降低巨噬细胞黏附油网络。在巨噬细胞粘附在纤连蛋白吸附的TCPS或网络上,而不是油纤连蛋白移植的网络上,这种纤连蛋白介导的粘附信号涉及RGD和PHSRN序列,其形式为TCPS上的G(3)RGDG(6)PHSRNG形式,而不是油网。此外,G(3)RGDG(6)PHSRNG嫁接到网络上引起巨噬细胞粘附的独特信号从预先吸附到网络上。因此,通过基质和配体结合方法来调节巨噬细胞的粘附和所选信号激酶的作用。 (C)2002 Elsevier Science Inc.保留所有权利。 [参考:30]

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