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首页> 外文期刊>Cell communication & adhesion >Heparin Modulates Integrin-Mediated Cellular Adhesion: Specificity of Interactions with α and β Integrin Subunits
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Heparin Modulates Integrin-Mediated Cellular Adhesion: Specificity of Interactions with α and β Integrin Subunits

机译：肝素调节整合素介导的细胞粘附：与α和β整合素亚基相互作用的特异性。

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Heparin is known to influence the growth, proliferation, and migration of vascular cells, but the precise mechanisms are unknown. We previously demonstrated that unfractionated heparin (UH) binds to the platelet integrin α_(IIb)β_3, and enhances ligand binding. To help define the specificity and site(s) of heparin-integrin interactions, we employed the erythroleukemic K562 cell line, transfected to express specific integrins (α_vβ_3, α_vβ_5, and α_(IIb)β_3). By comparing K562 cells expressing a common α subunit (Kα_vβ_3, Kα_vβ_5) with cells expressing a common β subunit (Kα_vβ_3, Kα_(IIb)β_3), we observed that heparin differentially modulated integrin-mediated adhesion to vitronectin. UH at 0.5-7.5 μg/ml consistently enhanced the adhesion of β_3 expressing cells (Kα_vβ_3,Kα_(IIb)β_3). In contrast, UH at 0.5-7.5 μg/ml inhibited Kα_vβ_5 adhesion. Experiments using integrin-blocking antibodies, appropriate control ligands, and nontransfected native K562 cells revealed that heparin's actions were mediated by the specific integrins under study. Preincubation of heparin with Kα_vβ_3 cells enhanced adhesion, while preincubation of heparin with the adhesive substrate (vitronectin) had minimal effect. There was a structural specificity to heparin's effect, in that a low molecular weight heparin and chondroitin sulfate showed significantly less enhancement of adhesion. These findings suggest that heparin's modulation of integrin-ligand interactions occurs through its action on the integrin. The inhibitory or stimulatory effects of heparin depend on the β subunit type, and the potency is dictated by structural characteristics of the glycosaminoglycan.
机译：已知肝素会影响血管细胞的生长，增殖和迁移，但确切的机制尚不清楚。我们先前证明，普通肝素（UH）与血小板整合素α_（IIb）β_3结合，并增强配体结合。为了帮助定义肝素与整联蛋白相互作用的特异性和位点，我们采用了转染表达特定整联蛋白（α_vβ_3，α_vβ_5和α_（IIb）β_3）的红白血病K562细胞系。通过比较表达共同α亚基（Kα_vβ_3，Kα_vβ_5）的K562细胞和表达共同β亚基（Kα_vβ_3，Kα_（IIb）β_3）的细胞，我们观察到肝素对整合素介导的对玻连蛋白的粘附性进行了差异调节。 0.5-7.5μg/ ml的UH持续增强表达β_3的细胞（Kα_vβ_3，Kα_（IIb）β_3）的粘附。相反，0.5-7.5μg/ ml的UH抑制Kα_vβ_5粘附。使用整合素阻断抗体，合适的对照配体和未转染的天然K562细胞进行的实验表明，肝素的作用是由所研究的特定整合素介导的。肝素与Kα_vβ_3细胞的预温育可增强粘附力，而肝素与粘合底物（玻连蛋白）的预温育作用最小。对肝素的作用具有结构特异性，因为低分子量肝素和硫酸软骨素显示出明显较少的粘附增强。这些发现表明，肝素对整联蛋白-配体相互作用的调节是通过其对整联蛋白的作用而发生的。肝素的抑制或刺激作用取决于β亚基类型，其效力由糖胺聚糖的结构特征决定。

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