Deficiency and Also Transgenic Overexpression of Timp-3 Both Lead to Compromised Bone Mass and Architecture In Vivo.

Tissue inhibitor of metalloproteinases-3 (TIMP-3) regulates extracellular matrix via its inhibition of matrix metalloproteinases and membrane-bound sheddases. Timp-3 is expressed at multiple sites of extensive tissue remodelling. This extends to bone where its role, however, remains largely unresolv...

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Main Authors: Behzad Javaheri, Mark Hopkinson, Blandine Poulet, Andrea S Pollard, Sandra J Shefelbine, Yu-Mei Chang, Philippa Francis-West, George Bou-Gharios, Andrew A Pitsillides
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2016-01-01
Series:PLoS ONE
Online Access:https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0159657&type=printable
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author Behzad Javaheri
Mark Hopkinson
Blandine Poulet
Andrea S Pollard
Sandra J Shefelbine
Yu-Mei Chang
Philippa Francis-West
George Bou-Gharios
Andrew A Pitsillides
author_facet Behzad Javaheri
Mark Hopkinson
Blandine Poulet
Andrea S Pollard
Sandra J Shefelbine
Yu-Mei Chang
Philippa Francis-West
George Bou-Gharios
Andrew A Pitsillides
author_sort Behzad Javaheri
collection DOAJ
description Tissue inhibitor of metalloproteinases-3 (TIMP-3) regulates extracellular matrix via its inhibition of matrix metalloproteinases and membrane-bound sheddases. Timp-3 is expressed at multiple sites of extensive tissue remodelling. This extends to bone where its role, however, remains largely unresolved. In this study, we have used Micro-CT to assess bone mass and architecture, histological and histochemical evaluation to characterise the skeletal phenotype of Timp-3 KO mice and have complemented this by also examining similar indices in mice harbouring a Timp-3 transgene driven via a Col-2a-driven promoter to specifically target overexpression to chondrocytes. Our data show that Timp-3 deficiency compromises tibial bone mass and structure in both cortical and trabecular compartments, with corresponding increases in osteoclasts. Transgenic overexpression also generates defects in tibial structure predominantly in the cortical bone along the entire shaft without significant increases in osteoclasts. These alterations in cortical mass significantly compromise predicted tibial load-bearing resistance to torsion in both genotypes. Neither Timp-3 KO nor transgenic mouse growth plates are significantly affected. The impact of Timp-3 deficiency and of transgenic overexpression extends to produce modification in craniofacial bones of both endochondral and intramembranous origins. These data indicate that the levels of Timp-3 are crucial in the attainment of functionally-appropriate bone mass and architecture and that this arises from chondrogenic and osteogenic lineages.
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spelling doaj-art-8c729571bc684693be70e8d6a47be8d62025-08-20T02:31:59ZengPublic Library of Science (PLoS)PLoS ONE1932-62032016-01-01118e015965710.1371/journal.pone.0159657Deficiency and Also Transgenic Overexpression of Timp-3 Both Lead to Compromised Bone Mass and Architecture In Vivo.Behzad JavaheriMark HopkinsonBlandine PouletAndrea S PollardSandra J ShefelbineYu-Mei ChangPhilippa Francis-WestGeorge Bou-GhariosAndrew A PitsillidesTissue inhibitor of metalloproteinases-3 (TIMP-3) regulates extracellular matrix via its inhibition of matrix metalloproteinases and membrane-bound sheddases. Timp-3 is expressed at multiple sites of extensive tissue remodelling. This extends to bone where its role, however, remains largely unresolved. In this study, we have used Micro-CT to assess bone mass and architecture, histological and histochemical evaluation to characterise the skeletal phenotype of Timp-3 KO mice and have complemented this by also examining similar indices in mice harbouring a Timp-3 transgene driven via a Col-2a-driven promoter to specifically target overexpression to chondrocytes. Our data show that Timp-3 deficiency compromises tibial bone mass and structure in both cortical and trabecular compartments, with corresponding increases in osteoclasts. Transgenic overexpression also generates defects in tibial structure predominantly in the cortical bone along the entire shaft without significant increases in osteoclasts. These alterations in cortical mass significantly compromise predicted tibial load-bearing resistance to torsion in both genotypes. Neither Timp-3 KO nor transgenic mouse growth plates are significantly affected. The impact of Timp-3 deficiency and of transgenic overexpression extends to produce modification in craniofacial bones of both endochondral and intramembranous origins. These data indicate that the levels of Timp-3 are crucial in the attainment of functionally-appropriate bone mass and architecture and that this arises from chondrogenic and osteogenic lineages.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0159657&type=printable
spellingShingle Behzad Javaheri
Mark Hopkinson
Blandine Poulet
Andrea S Pollard
Sandra J Shefelbine
Yu-Mei Chang
Philippa Francis-West
George Bou-Gharios
Andrew A Pitsillides
Deficiency and Also Transgenic Overexpression of Timp-3 Both Lead to Compromised Bone Mass and Architecture In Vivo.
PLoS ONE
title Deficiency and Also Transgenic Overexpression of Timp-3 Both Lead to Compromised Bone Mass and Architecture In Vivo.
title_full Deficiency and Also Transgenic Overexpression of Timp-3 Both Lead to Compromised Bone Mass and Architecture In Vivo.
title_fullStr Deficiency and Also Transgenic Overexpression of Timp-3 Both Lead to Compromised Bone Mass and Architecture In Vivo.
title_full_unstemmed Deficiency and Also Transgenic Overexpression of Timp-3 Both Lead to Compromised Bone Mass and Architecture In Vivo.
title_short Deficiency and Also Transgenic Overexpression of Timp-3 Both Lead to Compromised Bone Mass and Architecture In Vivo.
title_sort deficiency and also transgenic overexpression of timp 3 both lead to compromised bone mass and architecture in vivo
url https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0159657&type=printable
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