Related Experiment Video
Updated: Aug 8, 2026
14:48
Flow Cytometric Isolation of Primary Murine Type II Alveolar Epithelial Cells for Functional and Molecular Studies
Published on: December 26, 2012
Intercellular adhesion molecule-1 expression on the alveolar epithelium and its modification by hyperoxia
B H Kang1, J D Crapo, C D Wegner
1Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710.
American Journal of Respiratory Cell and Molecular Biology
|October 1, 1993
Summary
Intercellular adhesion molecule-1 (ICAM-1) is mainly on type I lung cells. Hyperoxia (100% O2) alters ICAM-1 distribution on type I cells and increases it on type II cells, potentially affecting neutrophil activity.
Area of Science:
- Pulmonary biology
- Cellular immunology
- Respiratory medicine
Background:
- Intercellular adhesion molecule-1 (ICAM-1) plays a role in immune cell interactions within the lung.
- Understanding ICAM-1 distribution is crucial for comprehending lung inflammation and injury.
Purpose of the Study:
- To investigate the distribution of ICAM-1 on alveolar epithelial cells.
- To determine the effects of hyperoxia (100% O2 exposure) on ICAM-1 expression in mouse lungs.
Main Methods:
- Electron microscopy immunocytochemistry was used to visualize ICAM-1.
- Immunoblot analysis quantified ICAM-1 levels.
- Mouse lungs were exposed to normoxia (air) or hyperoxia (100% O2) for 84 hours.
Main Results:
- In normal lungs, ICAM-1 was abundant on type I alveolar epithelial cells, particularly near cell junctions.
- Hyperoxia exposure abolished the ICAM-1 gradient near type I cell junctions.
- Hyperoxia markedly induced ICAM-1 expression on type II alveolar epithelial cells.
Conclusions:
- ICAM-1 is primarily located on type I epithelial cell surfaces near cell junctions in normal lungs.
- Hyperoxia significantly alters ICAM-1 distribution on type I cells and induces its expression on type II cells.
- These changes in ICAM-1 may influence neutrophil recruitment and retention in the alveolar space during hyperoxic lung injury.
Related Concept Videos
02:53Adaptive Mechanisms in Cancer Cells
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
01:24Regulation of Angiogenesis and Blood Supply
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
01:24Overview of Cell-Matrix Interactions
The extracellular matrix or ECM holds cells together to form a tissue and allows the cells within the tissue to communicate. ECM comprises proteins such as fibronectin, collagen, laminin, etc. The most abundant protein in this space is collagen. Collagen fibers are interwoven with carbohydrate-containing protein molecules called proteoglycans. ECM allows cell migration and provides a structural scaffold at cell adhesion that anchors the cell when the extracellular matrix proteins interact with...
01:26Alveoli and Alveolar Ducts
The respiratory zone of the human body, which stands in contrast to the conducting zone, comprises the structures that actively participate in the exchange of gases. The initiation of this zone is marked by the terminal bronchioles converging into respiratory bronchioles, the tiniest bronchiole classification. The respiratory bronchioles give way to the alveolar ducts that opens into a congregation of alveoli. Actively involved in gas exchange, alveoli resemble tiny sacs similar to clusters of...
01:10Atelectasis II: Pathophysiology
Atelectasis develops when alveoli lose their air and collapse inward. Because lung tissue is naturally elastic, these air sacs shrink rather than remaining open. Collapsed alveoli are no longer ventilated, reducing their role in gas exchange. Blood flow may continue in these regions, creating a ventilation–perfusion mismatch. Clinical findings include decreased breath sounds, dullness to percussion, reduced chest expansion, and decreased tactile fremitus as sound transmission through collapsed...
01:23Chronic Obstructive Pulmonary Disease II: Emphysema
Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.