The function of Hsp25 induced by compressing force in osteoblasts

Objectives: It is well known that appropriate occlusal force promotes bone formation around implants, whereas bone resorption develops under no mechanical stress or overstressing. We previously reported that heat shock protein 25 kDa ( Hsp25 ) , COX-2 mRNA and its protein level was up-regulated when the compressing force was directly loaded to a mouse osteoblast-like cell line ( MC3T3-E1 ) for 24 hours. Though the functions of Hsp25 have not been fully understood, it has been thought Hsp25 was acted on resistant to apoptosis. The purpose of this study was to clarify the function of Hsp25 induced by compressing force.

Materials and Methods: We examined that activation of caspase 3 in MC3T3-E1 cell knocked down Hsp25 by using siRNA when compressing force ( 294 Pa ) was loaded to it for 24 hours. And the cell number was counted in a similar condition by cell counting kit.

Results: Caspase 3 was activated when compressing force was directly loaded to MC3T3--1 cell knocked down Hsp25 by siRNA. Furthermore, the cell number was decreased in MC3T3-E1 which was knocked down Hsp25 by siRNA.

Conclusions: It is suggested that Hsp25 induced by compressing force acts on anti-apoptosis by suppression of the activation of caspase 3 in MC3T3-E1 cells.