Studies on growth plate chondrocytes in situ: cell proliferation and differentiation.
In man, attaining full longitudinal growth and skeletal maturity may go towards preventing later problems, such as osteoporosis. In farmed species, it is becoming increasingly apparent that muscle growth or the calcium demands for reproduction have outstripped the ability of the skeleton to provide both support and sufficient calcium. Thus, understanding the mechanisms that control longitudinal growth is of vital importance. Methods for studying chondrocyte proliferation and differentiation increasingly rely on the use of isolated cells, but these do not reproduce in vivo conditions. It is therefore necessary to be able to assess chondrocyte function in situ in order to understand fully the actions of possible growth promoters and therapeutic agents. The control of chondrocyte proliferation seems to be heavily dependent on GH, which probably acts directly on the resting and proliferating chondrocytes (Fig. 3). In the former, it seems to regulate the commitment of prechondrocytes to the proliferative state, but the mechanisms whereby it achieves this are unclear. What is also unclear is the proportion of growth that is GH dependent and how much, if at all, the control of IGF-I production by nutritional and other factors contributes to longitudinal growth. The in situ biochemical approach has provided strong evidence that both TGF-beta and the c-myc proto-oncogene are involved in chondrocyte differentiation and may be early markers of this process (Fig. 3). Indirect evidence exists to support a role for c-myc expression in chondrocyte differentiation, as TGF-beta has been reported to have its mechanisms of action modulated by c-myc expression.(ABSTRACT TRUNCATED AT 250 WORDS)
Loveridge
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Bone Growth and Metabolism Unit, Rowett Research Institute, Aberdeen, UK.
Farquharson
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C
D000818:Animals; D001715:Bird Diseases / Q000378:metabolism; D001717:Birds; D002356:Cartilage / Q000166:cytology*; D002454:Cell Differentiation / Q000502:physiology; D002455:Cell Division / Q000502:physiology; D013006:Growth Hormone / Q000502:physiology; D006132:Growth Plate / Q000166:cytology*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000502:physiology; D010009:Osteochondrodysplasias / Q000378:metabolism / Q000662:veterinary; D000090063:Proto-Oncogene Mas
C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone