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A Multi-Cue Bioreactor to Evaluate the Inflammatory and Regenerative Capacity of Biomaterials under Flow and Stretch
Published on: December 10, 2020
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Modulation of Endothelial Inflammation by Low and High Magnitude Cyclic Stretch
Yufeng Tian1, Grzegorz Gawlak1, James J O'Donnell1
1Lung Injury Center, Section of Pulmonary and Critical Medicine, Department of Medicine, University of Chicago, Chicago, Illinois 60637, United States of America.
Plos One
|April 30, 2016
Summary
Excessive mechanical ventilation causes lung endothelial cell inflammation via cyclic stretch (CS). High CS (18%) activates GEF-H1, increasing inflammatory markers and barrier dysfunction, unlike low CS (5%).
Area of Science:
- Pulmonary medicine
- Cellular biology
- Biomedical engineering
Background:
- Mechanical ventilation can harm lung endothelium.
- Mechanisms of ventilator-induced endothelial inflammation are unclear.
- Cyclic stretch (CS) is a key mechanical stressor.
Purpose of the Study:
- Investigate CS effects on pulmonary endothelial cell (EC) inflammation.
- Determine mechanisms of CS-induced EC inflammatory response.
- Examine roles of ICAM1, IL-8, and GEF-H1.
Main Methods:
- Exposed pulmonary ECs to 5% and 18% CS for 28-72 hours.
- Stimulated ECs with bacterial lipopolysaccharide (LPS).
- Assessed ICAM1, IL-8, and GEF-H1 expression; measured EC barrier integrity; used siRNA for GEF-H1 knockdown.
Main Results:
- 18% CS, not 5% CS, increased ICAM1, sICAM1, and IL-8.
- 18% CS augmented LPS-induced inflammation and EC barrier disruption.
- 18% CS induced GEF-H1 expression; GEF-H1 knockdown abolished CS-induced inflammation and barrier dysfunction.
Conclusions:
- Excessive mechanical stretch (18% CS) exacerbates pulmonary EC inflammation.
- CS-induced inflammation is mediated by GEF-H1.
- GEF-H1 is a key mediator of ventilator-induced endothelial dysfunction.
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