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The receptor for advanced glycation end products (RAGE) contributes to the progression of emphysema in mice

Sambamurthy, N and Leme, AS and Oury, TD and Shapiro, SD (2015) The receptor for advanced glycation end products (RAGE) contributes to the progression of emphysema in mice. PLoS ONE, 10 (3).

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Abstract

© 2015 Sambamurthy et al. Several recent clinical studies have implied a role for the receptor for advanced glycation end products (RAGE) and its variants in chronic obstructive pulmonary disease (COPD). In this study we have defined a role for RAGE in the pathogenesis of emphysema in mice. RAGE deficient mice (RAGE-/-) exposed to chronic cigarette smoke were significantly protected from smoke induced emphysema as determined by airspace enlargement and had no significant reduction in lung tissue elastance when compared to their air exposed controls contrary to their wild type littermates. The progression of emphysema has been largely attributed to an increased inflammatory cell-mediated elastolysis. Acute cigarette smoke exposure in RAGE-/- mice revealed an impaired early recruitment of neutrophils, approximately a 6-fold decrease compared to wild type mice. Hence, impaired neutrophil recruitment with continued cigarette smoke exposure reduces elastolysis and consequent emphysema.


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Details

Item Type: Article
Status: Published
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Sambamurthy, N
Leme, ASasl15@pitt.eduASL15
Oury, TDtdoury@pitt.eduTDOURY
Shapiro, SDsds33@pitt.eduSDS33
Contributors:
ContributionContributors NameEmailPitt UsernameORCID
EditorHudson, Barry I.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Date: 17 March 2015
Date Type: Publication
Journal or Publication Title: PLoS ONE
Volume: 10
Number: 3
DOI or Unique Handle: 10.1371/journal.pone.0118979
Schools and Programs: School of Medicine > Pathology
Refereed: Yes
PubMed ID: 25781626
Date Deposited: 12 May 2015 19:55
Last Modified: 02 Feb 2019 16:58
URI: http://d-scholarship.pitt.edu/id/eprint/24156

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