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Decreased laminin expression by human lung epithelial cells and fibroblasts cultured in acellular lung scaffolds from aged mice

Godin, Lindsay M.; Sandri, Brian J.; Wagner, Darcy E. LU ; Meyer, Carolyn M.; Price, Andrew P.; Akinnola, Ifeolu; Weiss, Daniel J. and Panoskaltsis-Mortari, Angela Panoskaltsis Mortari (2016) In PLoS ONE 11(3).
Abstract

The lung changes functionally and structurally with aging. However, age-related effects on the extracellular matrix (ECM) and corresponding effects on lung cell behavior are not well understood. We hypothesized that ECM from aged animals would induce aging-related phenotypic changes in healthy inoculated cells. Decellularized whole organ scaffolds provide a powerful model for examining how ECM cues affect cell phenotype. The effects of age on ECM composition in both native and decellularized mouse lungs were assessed as was the effect of young vs old acellular ECM on human bronchial epithelial cells (hBECs) and lung fibroblasts (hLFs). Native aged (1 year) lungs demonstrated decreased expression of laminins α3 and α4, elastin and... (More)

The lung changes functionally and structurally with aging. However, age-related effects on the extracellular matrix (ECM) and corresponding effects on lung cell behavior are not well understood. We hypothesized that ECM from aged animals would induce aging-related phenotypic changes in healthy inoculated cells. Decellularized whole organ scaffolds provide a powerful model for examining how ECM cues affect cell phenotype. The effects of age on ECM composition in both native and decellularized mouse lungs were assessed as was the effect of young vs old acellular ECM on human bronchial epithelial cells (hBECs) and lung fibroblasts (hLFs). Native aged (1 year) lungs demonstrated decreased expression of laminins α3 and α4, elastin and fibronectin, and elevated collagen, compared to young (3 week) lungs. Proteomic analyses of decellularized ECM demonstrated similar findings, and decellularized aged lung ECM contained less diversity in structural proteins compared to young ECM. When seeded in old ECM, hBECs and hLFs demonstrated lower gene expression of laminins α3 and α4, respectively, as compared to young ECM, paralleling the laminin deficiency of aged ECM. ECM changes appear to be important factors in potentiating agingrelated phenotypes and may provide clues to mechanisms that allow for aging-related lung diseases.

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publishing date
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publication status
published
in
PLoS ONE
volume
11
issue
3
publisher
Public Library of Science
external identifiers
  • scopus:84961159953
ISSN
1932-6203
DOI
10.1371/journal.pone.0150966
language
English
LU publication?
no
id
f66d483c-3768-4d3b-8b83-61881ffc5b5e
date added to LUP
2017-08-15 14:39:04
date last changed
2017-10-01 05:38:34
@article{f66d483c-3768-4d3b-8b83-61881ffc5b5e,
  abstract     = {<p>The lung changes functionally and structurally with aging. However, age-related effects on the extracellular matrix (ECM) and corresponding effects on lung cell behavior are not well understood. We hypothesized that ECM from aged animals would induce aging-related phenotypic changes in healthy inoculated cells. Decellularized whole organ scaffolds provide a powerful model for examining how ECM cues affect cell phenotype. The effects of age on ECM composition in both native and decellularized mouse lungs were assessed as was the effect of young vs old acellular ECM on human bronchial epithelial cells (hBECs) and lung fibroblasts (hLFs). Native aged (1 year) lungs demonstrated decreased expression of laminins α3 and α4, elastin and fibronectin, and elevated collagen, compared to young (3 week) lungs. Proteomic analyses of decellularized ECM demonstrated similar findings, and decellularized aged lung ECM contained less diversity in structural proteins compared to young ECM. When seeded in old ECM, hBECs and hLFs demonstrated lower gene expression of laminins α3 and α4, respectively, as compared to young ECM, paralleling the laminin deficiency of aged ECM. ECM changes appear to be important factors in potentiating agingrelated phenotypes and may provide clues to mechanisms that allow for aging-related lung diseases.</p>},
  articleno    = {e0150966},
  author       = {Godin, Lindsay M. and Sandri, Brian J. and Wagner, Darcy E. and Meyer, Carolyn M. and Price, Andrew P. and Akinnola, Ifeolu and Weiss, Daniel J. and Panoskaltsis-Mortari, Angela Panoskaltsis Mortari},
  issn         = {1932-6203},
  language     = {eng},
  month        = {03},
  number       = {3},
  publisher    = {Public Library of Science},
  series       = {PLoS ONE},
  title        = {Decreased laminin expression by human lung epithelial cells and fibroblasts cultured in acellular lung scaffolds from aged mice},
  url          = {http://dx.doi.org/10.1371/journal.pone.0150966},
  volume       = {11},
  year         = {2016},
}