OBJECTIVETo study the mechanism of promoting wound healing with mixed grafting of autologous and allogeneic microskin in rats.

METHODSFifteen male Wistar rats served as alloskin donor. Forty-five female SD rats with full-thickness skin defect served as recipients in the study. In part one experiment, 27 SD rats were randomly divided into group I (n = 9, without allogeneic microskin), group II (n = 9, with mixed grafting of allogeneic microskin at area expansion rate of 10:1); group III (n = 9, with mixed grafting of allogeneic microskin at area expansion rate of 10:3) with grafting with the same amount of autologous microskin at area expansion rate of 10:1. In part two experiment, 18 SD rats were also divided into group I (n = 6, with autologous microskin only); group II (n = 6, with mixed grafting of autologous and allogeneic microskin with area expansion rate of 20:1 and 20:3 respectively); group III (n = 6, with mixed grafting of autologous and allogeneic microskin with area expansion rate of 20:1 and 20:6, respectively). Biopsy samples were obtained from healed wound area of SD rats in each group at different time points after operation. The histological changes, epidermal thickness, and immunohistochemical staining of Integrin beta1 were observed.

RESULTS(1) HE staining showed the thickness of epidermis in each group increased obviously, and various amounts of mononuclear cell infiltration and different degrees of vasodilation appeared in the dermal layer during 2 - 4 weeks. (2) Epidermal thickness in group II and III of part one experiment were significantly thicker than that in group I during 2 - 4 weeks after operation (P < 0.05), and the similar result was also seen in part two experiment on 3 and 4 weeks after operation (P < 0.05). (3) A positive staining pattern for Integrin beta1 was seen in the suprabasal layers (especially in the spinous and granular layers) in all groups. In part one experiment, the expression of Integrin beta1 in group II and III were obviously higher than that in group I on 2 week after operation (P < 0.01), and the expression of Integrin beta1 in group II (10 982 +/- 2169) was also higher than that in group III (4240 +/- 512, P < 0.01); the expression of Integrin beta1 in group II was still higher than that in group I and III (P < 0.01) 3 and 4 weeks after operation. In part two experiment, the expression of Integrin beta1 in group III (1618 +/- 171) was higher than that in group I 3 weeks after operation (1060 +/- 146, P < 0.05).

CONCLUSIONThe ectopic and increased expression of Integrin beta1 was closely associated with the proliferation and differentiation of epidermal cells, wound reepithelialization and thickened epidermis in mixed grafting of autologous and allogeneic microskin. Integrin beta1 may be responsible in promoting wound healing.