We examined the cellular and molecular processes involved in patellar tendon healing following induced injury. A
wound was surgically created at the center of the patellar tendon of adult rats. The
wound site was examined at selected time intervals by immunohistochemical and in situ hybridization techniques. It was found that, between the 2nd and 7th day postoperation, fibroblast-like cells invaded the
wound site. DiI-labelling experiments suggested that the majority of cells that occupied the
wound originated from the edges of the
wound. Furthermore, immunohistochemical studies revealed that at the
wound site a meshwork of
fibronectin developed that can support the migration of the DiI-labelled cells. We also examined the spatial and temporal expression patterns of the growth arrest specific 2 (GAS2) gene during patellar tendon healing. GAS2 was found strongly expressed in the tenocytes of unoperated patellar tendons. The gene was also expressed in the intact regions of operated tendons but not in the fibroblast-like cells that occupied the
wound site, when examined 2 days postoperation. In addition the strip of intact tendon directly opposite the
wound site also did not express GAS2. Examination of the experimental tendon at the 3rd month, when cells had completely occupied the
wound site, revealed that Gas2 was expressed by all cells found in the
wound.
Bromodeoxyuridine (
BrdU) incorporation analysis revealed that the presence of
Brdu-positive cells in the
wound indirectly correlated with the absence of Gas2 expression. We speculate that the GAS2 gene might play a role in regulating tenocyte proliferation during tendon healing.