Sugahara H
Municipal Ikeda Hospital.
Nihon Rinsho. 1996 Jul;54(7):1809-14.
Little is known how Extra cellular matrix (ECM) molecules regulate proliferation of human hematopoietic progenitor cells. Fibronectin (FN) strikingly inhibited a human growth factor dependent cell line, M07E, cell proliferation. DNA content analysis revealed that FN treatment resulted in the appearance of subdiploid peak. Furthermore, FN induced oligonucleosomal DNA fragmentation and chromatin condensation, suggesting the involvement of apoptosis in the FN induced growth suppression. The apoptosis was rescued by anti-VLA5 mAb and the FN-induced apoptosis was detectable only VLA5-positive human cell lines but not in any of the VLA5-negative cell lines. These results suggest that FN induces apoptosis via its interaction with VLA5, and also raise the possibility that the FN-VLA5 interaction may contribute to negative regulation of hematopoiesis.
关于细胞外基质（ECM）分子如何调节人类造血祖细胞的增殖，人们知之甚少。纤连蛋白（FN）显著抑制了一种依赖人类生长因子的细胞系M07E的细胞增殖。DNA含量分析显示，FN处理导致亚二倍体峰的出现。此外，FN诱导了寡核小体DNA片段化和染色质浓缩，提示细胞凋亡参与了FN诱导的生长抑制。抗VLA5单克隆抗体可挽救这种细胞凋亡，且FN诱导的细胞凋亡仅在VLA5阳性的人类细胞系中可检测到，而在任何VLA5阴性的细胞系中均未检测到。这些结果表明，FN通过与VLA5相互作用诱导细胞凋亡，也增加了FN-VLA5相互作用可能参与造血负调控的可能性。
