Pepper M S, Spray D C, Chanson M, Montesano R, Orci L, Meda P
Department of Morphology, University of Geneva Medical Center, Switzerland.
J Cell Biol. 1989 Dec;109(6 Pt 1):3027-38. doi: 10.1083/jcb.109.6.3027.
Using an in vitro model in which a confluent monolayer of capillary endothelial cells is mechanically wounded, gap junction-mediated intercellular communication has been studied by loading the cells with the fluorescent dye, Lucifer Yellow. Approximately 40-50% of the cells in a nonwounded confluent monolayer were coupled in groups of four to five cells (basal level). Basal levels of communication were also observed in sparse and preconfluent cultures, but were reduced in postconfluent monolayers. 30 min after wounding, coupling was markedly reduced between cells lining the wound. Communication at the wound was partially reestablished by 2 h, exceeded basal levels after 6 h and reached a maximum after 24 h, at which stage approximately 90% of the cells were coupled in groups of six to seven cells. When the wound had closed (after 8 d), the increase in communication was no longer observed. Induction of wound-associated communication was unaffected by exposure of the cells to the DNA synthesis inhibitor mitomycin C, but was prevented by the protein synthesis inhibitor, cycloheximide. The induction of wound-associated communication was also inhibited when migration was prevented by placing the cells immediately after wounding at 22 degrees C or after exposure to cytochalasin D, suggesting that the increase in communication is dependent on cells migrating into the wound area. In contrast, migration was not prevented when coupling was blocked by exposure of the cells to retinoic acid, although this agent did disrupt the characteristic sheet-like pattern of migration typically seen during endothelial repair. These results suggest that junctional communication may play an important role in wound repair, possibly by coordinating capillary endothelial cell migration.
利用体外模型,在该模型中汇合的单层毛细血管内皮细胞受到机械损伤,通过用荧光染料鲁米诺黄加载细胞来研究间隙连接介导的细胞间通讯。在未受伤的汇合单层中,约40%-50%的细胞以四到五个细胞为一组相互耦联(基础水平)。在稀疏和预汇合培养物中也观察到基础通讯水平,但在汇合后单层中降低。损伤后30分钟,伤口边缘细胞之间的耦联明显减少。伤口处的通讯在2小时时部分恢复,6小时后超过基础水平,并在24小时时达到最大值,此时约90%的细胞以六到七个细胞为一组相互耦联。当伤口愈合(8天后)时,通讯增加不再被观察到。伤口相关通讯的诱导不受细胞暴露于DNA合成抑制剂丝裂霉素C的影响,但被蛋白质合成抑制剂环己酰亚胺阻止。当在损伤后立即将细胞置于22℃或暴露于细胞松弛素D后阻止迁移时,伤口相关通讯的诱导也受到抑制,这表明通讯的增加依赖于细胞迁移到伤口区域。相比之下,当细胞暴露于视黄酸而阻止耦联时,迁移并未被阻止,尽管该试剂确实破坏了内皮修复过程中通常可见的特征性片状迁移模式。这些结果表明,连接通讯可能在伤口修复中起重要作用,可能是通过协调毛细血管内皮细胞迁移。