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MT1-MMP–dependent, apoptotic remodeling of unmineralized cartilage

MT1-MMP–dependent, apoptotic remodeling of unmineralized cartilage Skeletal tissues develop either by intramembranous ossification, where bone is formed within a soft connective tissue, or by endochondral ossification. The latter proceeds via cartilage anlagen, which through hypertrophy, mineralization, and partial resorption ultimately provides scaffolding for bone formation. Here, we describe a novel and essential mechanism governing remodeling of unmineralized cartilage anlagen into membranous bone, as well as tendons and ligaments. Membrane-type 1 matrix metalloproteinase (MT1-MMP)–dependent dissolution of unmineralized cartilages, coupled with apoptosis of nonhypertrophic chondrocytes, mediates remodeling of these cartilages into other tissues. The MT1-MMP deficiency disrupts this process and uncouples apoptotic demise of chondrocytes and cartilage degradation, resulting in the persistence of “ghost” cartilages with adverse effects on skeletal integrity. Some cells entrapped in these ghost cartilages escape apoptosis, maintain DNA synthesis, and assume phenotypes normally found in the tissues replacing unmineralized cartilages. The coordinated apoptosis and matrix metalloproteinase-directed cartilage dissolution is akin to metamorphosis and may thus represent its evolutionary legacy in mammals. cranial vault; Meckel's cartilage; matrix dissolution; chondrocyte apoptosis; metamorphosis; MT1-MMP Footnotes K. Holmbeck and P. Bianco contributed equally to this work. Abbreviations used in this paper: MC, Meckel's cartilage; MMP, matrix metalloproteinase; MT1-MMP, membrane-type 1 MMP. Submitted: 10 July 2003 Accepted: 17 September 2003 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Cell Biology Rockefeller University Press

MT1-MMP–dependent, apoptotic remodeling of unmineralized cartilage

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References (56)

Publisher
Rockefeller University Press
Copyright
© 2003 Rockefeller University Press
ISSN
0021-9525
eISSN
1540-8140
DOI
10.1083/jcb.200307061
pmid
14610065
Publisher site
See Article on Publisher Site

Abstract

Skeletal tissues develop either by intramembranous ossification, where bone is formed within a soft connective tissue, or by endochondral ossification. The latter proceeds via cartilage anlagen, which through hypertrophy, mineralization, and partial resorption ultimately provides scaffolding for bone formation. Here, we describe a novel and essential mechanism governing remodeling of unmineralized cartilage anlagen into membranous bone, as well as tendons and ligaments. Membrane-type 1 matrix metalloproteinase (MT1-MMP)–dependent dissolution of unmineralized cartilages, coupled with apoptosis of nonhypertrophic chondrocytes, mediates remodeling of these cartilages into other tissues. The MT1-MMP deficiency disrupts this process and uncouples apoptotic demise of chondrocytes and cartilage degradation, resulting in the persistence of “ghost” cartilages with adverse effects on skeletal integrity. Some cells entrapped in these ghost cartilages escape apoptosis, maintain DNA synthesis, and assume phenotypes normally found in the tissues replacing unmineralized cartilages. The coordinated apoptosis and matrix metalloproteinase-directed cartilage dissolution is akin to metamorphosis and may thus represent its evolutionary legacy in mammals. cranial vault; Meckel's cartilage; matrix dissolution; chondrocyte apoptosis; metamorphosis; MT1-MMP Footnotes K. Holmbeck and P. Bianco contributed equally to this work. Abbreviations used in this paper: MC, Meckel's cartilage; MMP, matrix metalloproteinase; MT1-MMP, membrane-type 1 MMP. Submitted: 10 July 2003 Accepted: 17 September 2003

Journal

The Journal of Cell BiologyRockefeller University Press

Published: Nov 10, 2003

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