Analyzing autophagy in clinical tissues of lung and vascular diseases. Academic Article uri icon

Overview

MeSH

  • Animals
  • Blotting, Western
  • Cells, Cultured
  • Chromatin Immunoprecipitation
  • Endothelial Cells
  • Epithelial Cells
  • Fibroblasts
  • Mice
  • Microscopy, Electron, Transmission
  • Myocytes, Smooth Muscle

MeSH Major

  • Autophagy
  • Lung

abstract

  • Autophagy, a process by which organelles and cellular proteins are encapsulated in double-membrane vesicles and subsequently degraded by lysosomes, plays a central role in cellular and tissue homeostasis. In various model systems, autophagy may be triggered by nutrient deprivation, oxidative stress, and other insults such as endoplasmic reticulum stress, hypoxia, and pathogen infection. The role of autophagy in lung physiology and homeostasis, however, has not been well studied. Even less is known of the role of autophagy in the pathogenesis of chronic lung disease. Autophagy may act essentially as a protective mechanism in lung cells, by removing dysfunctional organelles, and recycling essential nutrients. On the other hand, excessive autophagy may also contribute to cell death pathways, resulting in the depletion of critical cell populations, and thus may also contribute to the disease pathogenesis. An understanding of the cell-type specific regulation and function of autophagy in the lung may facilitate the development of therapeutic strategies for the treatment of lung pathologies. This chapter provides protocols for the isolation of distinct lung cell types, such as epithelial, endothelial, macrophages, and fibroblasts; as well as protocols for the analysis of autophagy in lung cells and tissues.

publication date

  • 2009

has subject area

  • Animals
  • Autophagy
  • Blotting, Western
  • Cells, Cultured
  • Chromatin Immunoprecipitation
  • Endothelial Cells
  • Epithelial Cells
  • Fibroblasts
  • Lung
  • Mice
  • Microscopy, Electron, Transmission
  • Myocytes, Smooth Muscle

Research

keywords

  • Journal Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1016/S0076-6879(08)04010-X

PubMed ID

  • 19216908

Additional Document Info

start page

  • 197

end page

  • 216

volume

  • 453