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* Department of Anatomy and Histology, and Matrix vesicles have a critical role in the initiation of mineral deposition in skeletal tissues, but the
ways in which they exert this key function remain
poorly understood. This issue is made even more intriguing by the fact that matrix vesicles are also present
in nonmineralizing tissues. Thus, we tested the novel hypothesis that matrix vesicles produced and released
by mineralizing cells are structurally and functionally
different from those released by nonmineralizing cells.
To test this hypothesis, we made use of cultures of chick
embryonic hypertrophic chondrocytes in which mineralization was triggered by treatment with vitamin C and
phosphate. Ultrastructural analysis revealed that both
control nonmineralizing and vitamin C/phosphatetreated mineralizing chondrocytes produced and released matrix vesicles that exhibited similar round
shape, smooth contour, and average size. However, unlike control vesicles, those produced by mineralizing
chondrocytes had very strong alkaline phosphatase activity and contained annexin V, a membrane-associated protein known to mediate Ca2+ influx into matrix vesicles. Strikingly, these vesicles also formed numerous
apatite-like crystals upon incubation with synthetic cartilage lymph, while control vesicles failed to do so.
Northern blot and immunohistochemical analyses
showed that the production and release of annexin
V-rich matrix vesicles by mineralizing chondrocytes
were accompanied by a marked increase in annexin V
expression and, interestingly, were followed by increased expression of type I collagen. Studies on embryonic cartilages demonstrated a similar sequence of
phenotypic changes during the mineralization process
in vivo. Thus, chondrocytes located in the hypertrophic zone of chick embryo tibial growth plate were characterized by strong annexin V expression, and those located at the chondro-osseous mineralizing border exhibited expression of both annexin V and type I
collagen. These findings reveal that hypertrophic chondrocytes can qualitatively modulate their production of
matrix vesicles and only when induced to initiate mineralization, will release mineralization-competent matrix vesicles rich in annexin V and alkaline phosphatase.
The occurrence of type I collagen in concert with cartilage matrix calcification suggests that the protein may
facilitate crystal growth after rupture of the matrix vesicle membrane; it may also offer a smooth transition
from mineralized type II/type X collagen-rich cartilage
matrix to type I collagen-rich bone matrix.
Department of Biochemistry, School of Dental Medicine, University of
Pennsylvania, Philadelphia, Pennsylvania 19104
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