HSP 47 and Angiogenic Factor Expression and Its Implication for the Healing of Periosteal Defects in the Mouse Cranium

Abstract

We investigated collagen formation during healing in an experimentally-created periosteal defect site (PDS) in terms of the immunohistochemical detection of Heat Shock Protein 47 (HSP47) and-Smooth Muscle Actin (-SMA) along with the histopathological observation. In addition, we investigated expression of angiogenic factors, Vascular Endothelial Growth Factor (VEGF) and von Willebrand Factor (vWF), from the viewpoint of nutritional compensation for the bone in the PDS. The histological findings showed that the PDS was filled with fibrin-like structure until 3 days postoperatively, with granulation tissue at 5 days postoperatively, and it was finally replaced by collagenous fibers. The reparative periosteum-like tissue at 84 days postoperatively, showed features similar to those of normal periosteum. HSP47 and-SMA showed a positive reaction in fibroblast-like cells as well as immature collagen fibers in the healing process of the PDS. At 84 days after operation, some of the fibroblast-like cells in the reparative periosteum-like tissue showed a positive reaction to HSP47 and-SMA, similar to normal periosteum. Some collagen fibers in the normal periosteum showed a positive reaction for vWF. Fibrin-like structure, granulation tissue including fibrobast-like cells and some collagen fibers in the PDS were positive for VEGF and vWF during the experimental term. In conclusion, it is suggested that periosteal defects heal with regeneration of the collagenous structure, which has a role of nourishing the corresponding bone tissue.

Treatment of pancreatic fibrosis with siRNA against a collagen-specific chaperone in vitamin A-coupled liposomes

“…Regarding the mechanism for the enhanced microvascularity in fibrotic tissue and decrement of vascularity after treatment, we assume, in good agreement with reports by and Hideshima and Okada,23 24 that aPSCs are producing angiogenesis factor(s) which will be eradicated from the tissue in accordance with apoptosis induction by treatment. This assumption is based on our recent finding that rat aPSCs are indeed expressing some angiogenesis factors, including fibroblast growth factor (unpublished observation).…”