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Unlike epithelial tissue, which is composed of cells closely packed with little or no extracellular space in between, connective tissue cells are dispersed in a matrix. This extracellular matrix (ECM) is composed of fibrous proteins like collagen, elastin, and fibronectin in a ground substance consisting of interstitial fluid, cell adhesion proteins, and proteoglycans. The proteoglycans form a gel-like material in the spaces between cells and provide hydration, buffering, binding, and force...
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Techniques to Induce and Quantify Cellular Senescence
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Link between increased cellular senescence and extracellular matrix changes in COPD.

Roy R Woldhuis1,2,3,4, Maaike de Vries5,2, Wim Timens1,2

  • 1Department of Pathology and Medical Biology, University of Groningen, University Medical Centre Groningen, Groningen, The Netherlands.

American Journal of Physiology. Lung Cellular and Molecular Physiology
|May 29, 2020
PubMed
Summary

Chronic obstructive pulmonary disease (COPD) is linked to accelerated aging. Fibroblasts from COPD patients, including severe early-onset COPD, show increased cellular senescence, DNA damage, and oxidative stress, impacting extracellular matrix.

Keywords:
COPDECMSEO-COPDagingsenescence

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Area of Science:

  • Pulmonary Medicine
  • Aging Research
  • Cell Biology

Background:

  • Chronic obstructive pulmonary disease (COPD) exhibits accelerated aging features like cellular senescence and DNA damage.
  • Severe early-onset COPD (SEO-COPD) may show more pronounced aging characteristics.
  • The aging profile of fibroblasts in COPD, particularly SEO-COPD, and their impact on the extracellular matrix (ECM) remain largely uncharacterized.

Purpose of the Study:

  • To investigate aging markers in lung fibroblasts from SEO-COPD and older COPD patients.
  • To assess the impact of these aging features on ECM expression in COPD fibroblasts.
  • To validate COPD-related differences in senescence and ECM in lung tissue.

Main Methods:

  • Analysis of aging hallmarks (senescence, DNA damage, oxidative stress) and ECM markers in lung fibroblasts from SEO-COPD, older COPD, and matched non-COPD controls.
  • Comparison of fibroblasts under normal culture and after Paraquat-induced senescence.
  • Validation of findings in lung tissue samples.

Main Results:

  • COPD fibroblasts exhibited higher cellular senescence (SA-β-gal, p16), DNA damage (γ-H2A.X), and oxidative stress (MGST1) compared to controls.
  • SEO-COPD fibroblasts showed significant increases in SA-β-gal-positive cells compared to controls.
  • Lower decorin expression in COPD fibroblasts correlated with higher p16 expression, a finding confirmed in lung tissue.

Conclusions:

  • COPD fibroblasts, including those from SEO-COPD patients, display hallmarks of accelerated aging.
  • A potential link exists between cellular senescence and altered ECM expression in COPD.
  • These findings suggest ECM dysregulation may be associated with accelerated aging in COPD.