Effects of mechanical strain on bone metabolism in senescence accelerated mouse (SAM)

1999 Fiscal Year Final Research Report Summary

• Project/Area Number: 09470319
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Orthopaedic surgery
• Research Institution: University of the Ryukyus
• Principal Investigator: IBARAKI Kunio University of the Ryukyus, School of Medicine, Professor, 医学部, 教授 (00107187)
• Co-Investigator(Kenkyū-buntansha): OWAN Ichiro University of the Ryukyus, School of Medicine, Assistant Professor, 医学部, 助手 (80295310) ; YOSHIKAWA Tomoaki University of the Ryukyus, School of Medicine, Instructor, 医学部・附属病院, 講師 (10264491)
• Project Period (FY): 1997 – 1999
• Keywords: mechanotransduction / senescence accelerated mouse / osteoblast / bone formation

Research Abstract

Bone function is modulated by mechanical forces. The mechanism by which mechanical strain induces bone formation remains unclear. SAM-P/6 is a novel murine model of senile osteoporosis which is characterized by low peak bone mass. In contrast, SAM-R/1 is a strain with high peak bone mass. To study the effects of mechanical strain on bone metabolism and identify a novel gone which is involved in mechanotransduction, the bone formation response to mechanical strain is compared between SAM-P/6 and SAM-R/1.
Mechanical loading increased the expression of several factors such as COX-2, c-fos, and osteopontin mRNA much higher in SAM-R/1 than SAM-P/6 derived osteoblasts. However, a novel gene which is upregulated by mechanical loading in SAM-R/1 but not in SAM-P/6 could not be identified so far, and still under investigation.