Hypertrophy of growth plate chondrocytes in vivo is accompanied by modulations in the activity state and surface area of their cytoplasmic organelles.
The rate of longitudinal bone growth is regulated primarily by modulations in the activity of epiphyseal plate hypertrophic chondrocytes, these being manifested as changes in cell and matrix volume. It was the purpose of this study to ascertain whether the cytoplasmic organelles representing the cellular production apparatus, i.e. rough endoplasmic reticulum, Golgi apparatus and mitochondria, contribute to these changes by modulating their rate of activity or by increasing/decreasing the surface area and/or volume of their membranes. Using rats at different stages of growth, the surface areas and volumes of the three organellar systems were quantified in epiphyseal plate chondrocytes at the onset and termination of hypertrophy by ultrastructural stereology. Matrix synthesis during the same span was assessed by monitoring the production of its principal components, namely, fibrillar collagen (ultrastructural morphometry) and glycosaminoglycans (quantitative (35)S-autoradiography). Each organelle adapts to increases (21- to 35-day-old rats) and decreases (35- to 80-day-old rats) in growth rate by its own individual combination of the two alternative mechanisms, but modulations in the level of activity predominate over alterations in the surface area or volume of their membranes. These findings point to the danger of relying solely on data gleaned from a quantitative ultrastructural analysis of organellar parameters and emphasise the necessity of conducting functional assays in parallel, as performed here.
Hunziker
E B
EB
M.E. Müller-Institute for Biomechanics, University of Bern, P.O. Box 30, CH-3010 Bern, Switzerland,
Kapfinger
E
E
Saager
C
C
D000818:Animals; D019902:Chondrocytes / Q000378:metabolism*; D003094:Collagen / Q000378:metabolism*; D003593:Cytoplasm / Q000378:metabolism; D005260:Female; D006025:Glycosaminoglycans / Q000378:metabolism*; D006132:Growth Plate / Q000378:metabolism* / Q000473:pathology; D015576:Hyperostosis / Q000378:metabolism* / Q000473:pathology; D015388:Organelles / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013977:Tibia / Q000378:metabolism / Q000473:pathology
D006025:Glycosaminoglycans; D003094:Collagen