Health Research Institute, Tissue Engineering Research Group, National Institute of Advanced Industrial Science and Technology, Nakouji, Amagasaki, Hyogo, Japan.
Cell Adh Migr. 2011 Mar-Apr;5(2):119-32. doi: 10.4161/cam.5.2.13908. Epub 2011 Mar 1.
CD43/sialophorin/leukosialin, a common leukocyte antigen, is known as an inhibitor for cell adhesion. The ectodomain of CD43 is considered as a molecular barrier for cell adhesion, while the cytoplasmic domain has a binding site for Ezrin/Radixin/Moesin (ERM). We found expression of CD43 induced cell rounding, inhibition of cell re-attachment, augmentation of microvilli, and phosphorylation of ERM in HEK293T cells. Mutant studies revealed the ectodomain of CD43, but not the intracellular domain, essential and sufficient for all these phenomena. We also found that forced cell detachment by itself induced phosphorylation of ERM in HEK293T cells. Taken together, these findings indicate that inhibition of cell adhesion by the ectodomain of CD43 induces phosphorylation of ERM, microvilli formation, and eventual cell rounding. Furthermore, our study suggests a novel possibility that cell detachment itself induces activation of ERM and modification of cell shape.
CD43/sialophorin/leukosialin,一种常见的白细胞抗原,被认为是一种细胞黏附抑制剂。CD43 的胞外域被认为是细胞黏附的分子屏障,而胞质域则有 Ezrin/Radixin/Moesin (ERM) 的结合位点。我们发现 CD43 的表达诱导细胞变圆、抑制细胞再附着、增加微绒毛、并使 ERM 磷酸化。突变研究表明,CD43 的胞外域而非胞内域,对于所有这些现象都是必需且充分的。我们还发现,细胞自身的强制分离本身就会诱导 HEK293T 细胞中 ERM 的磷酸化。综上所述,这些发现表明 CD43 的胞外域抑制细胞黏附会诱导 ERM 的磷酸化、微绒毛形成,最终导致细胞变圆。此外,我们的研究还提示了一种新的可能性,即细胞分离本身会诱导 ERM 的激活和细胞形态的改变。