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目的：探讨可溶性纤维蛋白（ Ｓ Ｆ）使细胞粘附伸展的可能性及其机理。方法：利用 Ｓｅｐｈａｃｒｙｌ Ｓ３００ 层析柱及 Ｉ Ｆ１ 单克隆抗体亲和层析柱纯化血浆 Ｓ Ｆ。应用细胞粘附及粘附抑制方法观察 Ｓ Ｆ及弥散性血管内凝血（ Ｄ Ｉ Ｃ）患者血浆 Ｓ Ｆ使细胞伸展的情况。结果：细胞能在固定的 Ｓ Ｆ上伸展，并能被外源性 Ｓ Ｆ精氨酸甘氨酸天冬氨酸（ Ｒ Ｇ Ｄ）合成肽所抑制，但不能被纤维蛋白原和纤维蛋白单体所抑制，片段 Ｘ（缺乏 Ｒ Ｇ Ｄ２ 序列的纤维蛋白原片段）与纤维蛋白单体形成的复合物，使细胞伸展活性明显减低。结论： Ｓ Ｆ形成后其结构变化是引起细胞伸展的关键。在 Ｓ Ｆ结构中，纤维蛋白原的 Ｒ Ｇ Ｄ２ 序列在细胞伸展中起重要作用。 Ｓ Ｆ做为一个粘附分子在体内血栓形成过程中起重要调节作用。
Objective: To investigate the possibility and mechanism of soluble fibrin (S F) cell adhesion and extension. Methods: The plasma S F was purified by Sephacryl S300 column and I F1 monoclonal antibody affinity chromatography. Cell adhesion and adherence inhibition methods were used to observe the S F and disseminated intravascular coagulation (D I C) patients with plasma S F cell extension situation. RESULTS: The cells were able to stretch at a fixed SS and were inhibited by the exogenous S F-Arginine-Glycine-Aspartate (RGD) synthetic peptide but not by fibrinogen and fibrin The complex formed by Fragment X (a fibrinogen fragment lacking the R G D2 sequence) and fibrin monomers inhibits cell spreading activity significantly. Conclusion: The structural change of S F after its formation is the key to cell expansion. In the SS structure, the RGD2 sequence of fibrinogen plays an important role in cell elongation. S F as an adhesion molecule plays an important regulatory role in thrombosis in vivo.