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First published online February 23, 2005

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Bone growth: the integrin connection

Most mammalian skeletal bones are formed by endochondral ossification – the replacement of a cartilaginous mould by bone. Cartilage development depends on the integrin-mediated interaction of the collagen-forming chondrocytes with the surrounding extracellular matrix. 10ß1 is the major integrin mediating this interaction and mice lacking ß1 integrin develop severe bone defects. Surprisingly, Reinhard Fässler and colleagues now report that mice lacking 10 integrin exhibit only slightly retarded growth of the long bones, which is caused by mild defects in the growth plate, a specialized structure in long bones that is responsible for linear bone growth (see p. 929). These defects include abnormalities in chondrocyte arrangement, shape and proliferation. In addition, the density of the collagen fibrillar network in these mice is reduced compared with that in normal mice. The authors conclude that integrin 10ß1 is important but not essential for endochondral ossification, presumably because other collagen-binding integrins, such as 2ß1, compensate for its loss, something that cannot happen in ß1-integrin-null mice.

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Loss of 10ß1 integrin expression leads to moderate dysfunction of growth plate chondrocytes

Therese Bengtsson, Attila Aszodi, Claudia Nicolae, Ernst B. Hunziker, Evy Lundgren-Åkerlund, and Reinhard Fässler
JCS 2005 118: 929-936. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?