1998 Fiscal Year Final Research Report Summary
Immunohistochemical Detection of Activin A,Follistatin, and Activin Receptors during Fracture Healing in the Rat
| Project/Area Number |
09671504
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kagoshima University |
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Principal Investigator |
SAKOU Takashi Faculty of Medicine Kagoshima University, Professor, 医学部, 教授 (10041295)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUNAGA Shunji University Hospital Kagoshima University, Assistant Professor, 医学部・附属病院, 講師 (90229500)
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| Project Period (FY) |
1997 – 1998
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| Keywords | fracture healing / activin / activin receptors / follistatin |
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| Research Abstract |
Activins are multifunctional proteins that belong to the transforming growth factor-B superfamily and are thought to play an important role in modulatin the formation of bone. Activins exert their cellular effects by way of activin type-I and type-IL serine/threonine kinase receptors. Follistatin is an activin-binding protein that can suppress the biological effects of aetivins. In this study, the immunohistochemical expression of activin A, follistatin, and activin receptors was studied during fracture healing in the rat. Activin A was weakly detected in the periosteum near the fracture ends at an early stage but was absent in the chondrocytes around the fracture gap, where endochondral ossification took place. An antibody to follistatin stained osteogenic cells in the periosteum near the fracture ends ; moderate and strong staining were observed in proliferating, mature, and hypertrophied chondrocytes at the sites of endochondral ossification. Levels of activin A and follistatin were high near the osteoblasts on the surface of the newly formed trabecular bone. In addition, an intense localization of activin A was noted where multinucleated ostcoclast-like cells were present. This study suggests that the activin-follistatin system may contribute to cellular events related to the formation and remodeling of bone during fracture healing. Activin type-I and type-IL receptors were co-expressed in intramembranous and endochondral ossification sites. The expression of activin type-I, type-II, and type-IIB receptors in the absence of activin A in the endochondral ossification suggests that other isoforms of activins may signal by way of these receptors.
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