Cell contact-dependent signaling is a major regulatory mechanism in the organization of developing tissues and in the reorganization (post-injury responses) of specialized tissues in multicellular organisms. In this review we contribute to the further understanding of post-injury recovery processes in adult nervous tissue. We emphasize evidence that supports the involvement of cell contact-inhibition signaling in the cell proliferation, growth and differentiation that occurs during healing and neural reorganization after brain damage.

A number of reports suggest that the process of ageing impairs wound repair and that strategies to manipulate the age-related wound healing environment are necessary in order to stimulate repair. The process of cutaneous wound repair is controlled by growth factors in an autocrine and paracrine fashion: it is therefore surprising that the localisation of specific growth factors and their receptors has not been documented in wound healing with respect to chronological age. In this study the temporal profile of growth factor and receptor immunostaining was assessed within acute incisional wounds in an ageing mouse colony. A delay in appearance of platelet derived growth factor (PDGF) A and B isoforms, and PDGF-α and -β receptors was evident with increasing animal age, paralleled by a similar finding for epidermal growth factor (EGF) and EGF receptor. Transforming growth factor (TGF)-7beta;1 and 2 isoforms were increased at all time points in the wounds of younger animals, but the TGF-β3 isoform increased in intensity from d 7 postwounding in the old mice wounds, and basic fibroblast growth factor (bFGF) from d 14. The quantity and distribution patterns of the various growth factors and their receptors may explain the age-related differences in wound healing speed and quality, and possibly suggest new therapeutic targets for manipulating wound healing in the aged.