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Lung ischemia: a model for endothelial mechanotransduction
Shampa Chatterjee1, Kenneth E Chapman, Aron B Fisher
1Institute for Environmental Medicine, University of Pennsylvania Medical Center, 1 John Morgan Building, 3620 Hamilton Walk, Philadelphia, PA, 19104-6068, USA.
Cell Biochemistry and Biophysics
|November 5, 2008
Summary
Endothelial cells respond to reduced blood flow by producing reactive oxygen species (ROS) and nitric oxide (NO), initiating signaling pathways that promote cell proliferation and blood vessel growth.
Area of Science:
- Cardiovascular Biology
- Cellular Mechanotransduction
- Endothelial Cell Physiology
Background:
- Endothelial cells are constantly exposed to blood flow-induced shear stress, which influences cellular functions through mechanotransduction.
- Altered shear stress, particularly its removal during ischemia, triggers specific cellular responses critical for tissue homeostasis.
Purpose of the Study:
- To review the role of shear sensors and signal transducers in endothelial cell responses to shear stress.
- To focus on the cellular mechanisms activated by the removal of shear stress, as observed in pulmonary ischemia.
Main Methods:
- Review of existing literature on endothelial cell mechanotransduction and response to ischemia.
- Analysis of studies using isolated murine lungs and pulmonary microvascular endothelial cells in vitro to investigate shear stress removal.
Main Results:
- Pulmonary ischemia induces endothelial generation of reactive oxygen species (ROS) and nitric oxide (NO).
- This response necessitates functional caveolae and involves endothelial cell depolarization, K(ATP) channel closure, and activation of NADPH oxidase (NOX2) and NO synthase (eNOS).
- Signaling pathways, including MAP kinases, mediate endothelial cell proliferation, vasodilation, and angiogenesis.
Conclusions:
- Endothelial cells possess intricate mechanisms to respond to compromised blood flow.
- These responses, involving ROS, NO, and specific signaling cascades, are crucial for compensatory vasodilation and angiogenesis to restore tissue perfusion.
