中文摘要：

为阐明整合素β3亚单位胞内区及其不同保守序列在骨桥蛋白（OPN）诱导血管平滑肌细胞（VSMC）黏附和迁移中所起的作用，构建了整合素β3亚单位胞内区肽段真核表达载体（PEGFP-C3-β3 CD），并人工合成了含有β3亚单位胞内区不同保守序列（NXXY）的寡肽（肽-747和肽-759），通过导入VSMC，观察它们对OPN诱导VSMC黏附和迁移的影响．结果显示，整合素β3胞内区在VSMC中强制性表达可使细胞在OPN上的黏附和迁移明显下降（分别为对照组的34．3％和31．7％）；导入肽-747、肽-759和肽-747＋肽-759均可显著抑制VSMC的黏附和迁移，其中肽-747＋肽-759的作用更强（分别为对照组的36．4％和31、1％）．免疫荧光结果显示，在转染PEGFP-C3-β3CD或肽-747＋肽-759的VSMC中，黏着斑蛋白的磷酸化水平降低，黏着斑形成明显减少．研究结果表明，整合素β3亚单位胞内区及其NXXY保守序列在黏着斑相关蛋白募集、黏着斑形成及VSMC黏附和迁移方面发挥重要作用．

英文摘要：

To investigate the effect of cytoplasmic domain of the integrin β3 subunit and its conserved NXXY motif on the adhension and migration of vascular smooth muscle cells （VSMCs） induced by osteopontin （OPN）, the eukaryotic expression vector, pEGFP-C3-β3CD, harboring the cytoplasmic domain of human integrin β3 subunit eDNA was constructed and the peptide-747 and peptide-759 including the NXXY motif were synthesized. Thereafter, they were transfected into VSMCs. The results showed that compared with control, the adhension and migration of VSMCs induced by OPN were obviously decreased to 34.3 % and 31.7%, respectively, when the cytoplasmic domain of integrin β3 was overexpressed in these cells. And these two activities of VSMCs were also inhibited by transfection of peptide-747, peptide-759. Especially, cotransfection of peptide-747＋peptide-759 markedly down-regulated the adhesion and migration of VSMC to 36.4 % and 31.1%, respectively, compared with control. Immunofluorescence revealed lower phosphorylation of focal adhension proteins and fewer number of focal adhension in VSMCs transfected by pEGFP-C3-β3-CD or peptide-747 ＋ peptide-759 comparing with control. These results suggest that the cytoplasmic domain of integrin β3 subunit could play a key role in the recruitment of focal adhension-related protein, then the formation of focal adhension and the adhension and migration of VSMCs through the conserved NXXY motif.