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Immunohistochemical detection of activin A, follistatin, and activin receptors during fracture healing in the rat
Author(s) -
Nagamine Tomonori,
Imamura Takeshi,
Ishidou Yasuhird,
Kato Mitsuyasu,
Murata Fusayoshi,
Dijke Peter ten,
Sakou Takashi
Publication year - 1998
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.1100160307
Subject(s) - follistatin , activin type 2 receptors , immunohistochemistry , receptor , activin receptor , wound healing , acvr2b , medicine , endocrinology , microbiology and biotechnology , tgf beta signaling pathway , chemistry , biology , immunology
Activins are multifunctional proteins that belong to the transforming growth factor‐β superfamily and are thought to play an important role in modulating the formation of bone. Activins exert their cellular effects by way of activin type‐I and type‐II serine/threonine kinase receptors. Follistatin is an activin‐binding protein that can suppress the biological effects of activins. 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 posteoblasts on the surface of the newly formed trabecular bone. In addition, an intense localization of activin A was noted where multinucleated osteoclast‐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‐II 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.