細胞の死に関する上皮細胞の反応

Epithelial cells are connected each other, cover our body and make compartments separated from surrounding environment. The tight junction, one of typical cell-to-cell junctions regulates flow of substances through cell gaps in epithelial cell sheets. This is called a barrier function of epithelial sheets. When this barrier function becomes weak due to wound, death of a part of cells constituting epithelial sheets, living cells surrounding the dead cells quickly accumulate actomyosin at the live/dead interphases within several minutes, forming an actomyosin ring surrounding dead cells. Contraction of this ring helps wound closure and extrusion of dead cells. It takes less than 1 hour to close the wound when only single cell is dead. After the completion of the closure, concentrated actomyosin quickly disappears along with formation of new tight junctions. Although cells can close the wound by migration of surrounding cells, this contraction of actomyosin ring is effective for closure and specific to epithelial cells with tight junctions. Signals stimulating the accumulation of actomyosin have been sought for decades, with no important candidate. Tight junction components, ZO-1 and ZO-2 are known to be essential for tight junction formation. Interestingly, loss of both ZO-1 and ZO-2 caused high accumulation of actomyosin at cell-cell interphases. It is possible that ZO-1/-2 in tight junctions reduce myosin activity near tight junctions. Loss of ZO-1/-2 may induce myosin activation and accumulation. Molecular analyses along this line would be essential for understanding the early signaling cascade leading to wound responses.