Re-epithelialisation and the possible involvement of the transcription factor, basonuclin.

This article briefly summarises the basic mechanism of re-epithelialisation and discusses the possible role of the cell-type-specific transcription factor, basonuclin. Re-epithelialisation is initiated by a signal resulting from the absence of neighbouring cells at the wound edge. Basal cells at the wound edge become flattened and lose their intercellular desmosomes and substratum attachment. The amount of cytoplasmic actinomyosin filaments that insert into the new adhesion complexes is increased, and contraction of those filaments produces cell movement. The epithelial cells at the wound edge migrate on a provisional matrix using the newly expressed integrin receptors. Once re-epithelialisation is complete, the epithelial cells revert to the normal phenotype of basal epidermal cells, firmly attach to the newly developed basement membrane zone through hemidesmosomes and resume standard differentiation. Protein synthesis increases in the epidermal cells at the wound edge during re-epithelialisation. Active protein synthesis requires accelerated transcription of ribosomal RNA genes. The transcription factor basonuclin binds to the ribosomal RNA gene promoter and increases the transcription of the genes. Therefore, it is speculated that basonuclin in epithelial cells is required in the process of re-epithelialisation.