Title of article :
Distribution of plasma-membrane Ca2+ pump in mandibular condyles from growing and adult rabbits
Author/Authors :
Sharawy، نويسنده , , Mohamed M and Kang، نويسنده , , Ki Ho and Kim، نويسنده , , Kyung.-Wook and Borke، نويسنده , , James L، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2000
Pages :
9
From page :
237
To page :
245
Abstract :
Chondrocytes may control the mineralization of the extracellular matrix of condylar cartilage by several mechanisms including the release of microvesicles involved in the initial nucleation, the creation or modification of the local matrix to help propagate or restrict mineralization, and the regulation of the ionic environment at the calcifying foci within the matrix. The plasma membrane Ca2+–Mg2+ ATPase (Ca2+ pump) is known to play a part in the vectorial efflux of calcium in a variety of cells including chondrocytes. The purpose here was to study the distribution of Ca2+-pump protein in mandibular condyles from growing and adult rabbits, and compare the expression of that protein in progressively differentiating chondrocytes whose final stage is associated with a mineralized extracellular matrix. Ca2+-pump antigen was identified immunohistochemically in six growing and six adult rabbit mandibular condyles with a Ca2+pump-specific monoclonal antibody. The presence of Ca2+-pump antigen was established in hypertrophic chondrocytes, and in osteoblasts and osteoclasts of subchondral bone. Slot-blot analysis of nitrocellulose-immobilized chondrocyte homogenates showed that the amount of Ca2+pump in growing cartilage was more than twice that in adult cartilage (p<0.05). The demonstration of Ca2+-pump antigen in the hypertrophic chondrocytes of growing rabbit condyles is consistent with a role for the plasma-membrane Ca2+ pump in the calcification of mandibular condylar cartilage.
Keywords :
Ca2+pump , Cartilage , calcification
Journal title :
Archives of Oral Biology
Serial Year :
2000
Journal title :
Archives of Oral Biology
Record number :
1801579
Link To Document :
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