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研究了蛋白质酪氨酸磷酸化在hTNF-α诱导猪主动脉内皮细胞(PAEC)黏附分子E-选择素(E-selectin)和血管细胞黏附分子-1(VCAM-1)表达以及在增强人外周血单核细胞(PBMo)和自然杀伤细胞(PBNK)黏附中的作用. 以选择性的蛋白质酪氨酸激酶(PTKs)抑制剂genistein预处理PAEC, 剂量依赖性地抑制了hTNF-α增强的PAEC对PBMo和PBNK的黏附. 这种抑制作用发生在hTNF-α激活PAEC的早期, 并且具有可恢复性. PTKs活性测定表明genistein剂量也依赖性地抑制了hTNF-α对PAEC的PTKs的激活. 流式细胞术PAEC表型分析指出genistein抑制了hTNF-α诱导的E-selectin和VCAM-1的表达. 这些结果表明PTKs可以调节hTNF-α诱导的PAEC黏附分子E-selectin和VCAM-1的表达, 以及hTNF-α增强PBMo和PBNK的黏附, 而饮食来源的genistein可能会作为一种黏附拮抗剂在控制这种细胞介导的排斥应答中发挥作用.
The effects of protein tyrosine phosphorylation on the expression of E-selectin and VCAM-1 on hTNF-α-induced porcine aortic endothelial cells (PAECs) (PBMo) and natural killer (PBNK) adhesion.PeECs were pretreated with genistein, a selective protein tyrosine kinase (PTKs) inhibitor, in a dose-dependent manner to inhibit hTNF-α-enhanced PAEC Adhesion to PBMo and PBNK This inhibition occurs early in the activation of PAEC by hTNF-α and is recoverable PTKs activity assay shows that genistein dose-dependently inhibits PTEN activation of PAEC by hTNF-α. PAEC phenotype analysis indicated that genistein inhibited the expression of E-selectin and VCAM-1 induced by hTNF-α. These results indicate that PTKs can regulate the expression of E-selectin and VCAM-1 induced by hTNF-α, And hTNF-α enhances PBMo and PBNK adhesion, whereas diet-derived genistein may play a role as an adhesion antagonist in controlling this cell-mediated rejection response.