Linked Life Data

12634787

Source:http://linkedlifedata.com/resource/pubmed/id/12634787

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pubmed-article:12634787pubmed:abstractTextIntegrins are heterodimeric cell-surface proteins that regulate cell growth, migration and survival. We have shown previously that the epithelial-restricted integrin alpha(v)beta6 has another critical function; that is, it binds and activates latent transforming growth factor-beta (TGF-beta). Through a global analysis of pulmonary gene expression in the lungs of mice lacking this integrin (Itgb6 null mice) we have identified a marked induction of macrophage metalloelastase (Mmp12)--a metalloproteinase that preferentially degrades elastin and has been implicated in the chronic lung disease emphysema. Here we report that Itgb6-null mice develop age-related emphysema that is completely abrogated either by transgenic expression of versions of the beta6 integrin subunit that support TGF-beta activation, or by the loss of Mmp12. Furthermore, we show that the effects of Itgb6 deletion are overcome by simultaneous transgenic expression of active TGF-beta1. We have uncovered a pathway in which the loss of integrin-mediated activation of latent TGF-beta causes age-dependent pulmonary emphysema through alterations of macrophage Mmp12 expression. Furthermore, we show that a functional alteration in the TGF-beta activation pathway affects susceptibility to this disease.lld:pubmed
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pubmed-article:12634787pubmed:articleTitleLoss of integrin alpha(v)beta6-mediated TGF-beta activation causes Mmp12-dependent emphysema.lld:pubmed
pubmed-article:12634787pubmed:affiliationLung Biology Center, Department of Medicine, San Francisco General Hospital, San Francisco, California 94143, USA.lld:pubmed
pubmed-article:12634787pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12634787pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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