Signaling pathway for nitric oxide generation with simulated ischemia in flow-adapted endothelial cells.
@article{Wei2001SignalingPF,
title={Signaling pathway for nitric oxide generation with simulated ischemia in flow-adapted endothelial cells.},
author={Z Wei and Abu-Bakr Al-Mehdi and Aron B. Fisher},
journal={American journal of physiology. Heart and circulatory physiology},
year={2001},
volume={281 5},
pages={
H2226-32
}
}Ischemia in the intact ventilated lung (oxygenated ischemia) leads to endothelial generation of reactive oxygen species (ROS) and nitric oxide (NO). This study investigated the signaling pathway for NO generation with oxygenated ischemia in bovine pulmonary artery endothelial cells (BPAEC) that were flow adapted in vitro. BPAECs were cultured in an artificial capillary system and subjected to abrupt cessation of flow (ischemia) under conditions where cellular oxygenation was maintained…
41 Citations
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References
SHOWING 1-10 OF 42 REFERENCES
Simulated ischemia in flow-adapted endothelial cells leads to generation of reactive oxygen species and cell signaling.
- BiologyCirculation research
- 1999
It is concluded that flow-adapted endothelial cells generate ROS with ischemia that results in activation of NF-kappaB and AP-1 and an increase of DNA synthesis and this effect is not mediated by hypoxia, implicating a role for mechanotransduction in ischemIA-mediated cell signaling.
Oxidative burst and NO generation as initial response to ischemia in flow-adapted endothelial cells.
- BiologyAmerican journal of physiology. Heart and circulatory physiology
- 2001
Flow-adapted endothelial cells sense the altered hemodynamics associated with flow cessation and respond by plasma membrane depolarization, activation of NADPH oxidase, Ca(2+) influx, and activation of Ca( 2+)/calmodulin-dependent NO synthase.
Ca2+- and Phosphatidylinositol 3-Kinase-dependent Nitric Oxide Generation in Lung Endothelial Cells in Situ with Ischemia*
- BiologyThe Journal of Biological Chemistry
- 2000
The similarity of endothelial cell response (increased NO generation) to either increased flow or cessation of flow suggests that cells respond to an imposed alteration from a state of adaptation.
Endothelial NADPH oxidase as the source of oxidants in lungs exposed to ischemia or high K+.
- Biology, ChemistryCirculation research
- 1998
It is demonstrated that ROS production in lungs exposed to ischemia or high K+ results from assembly and activation of a membrane-associated NAPDH oxidase of the pulmonary endothelium, and the increased dichlorofluorescein fluorescence in these models of ROS generation was localized primarily to the pulmonary artery endothelial cells.
Shear-induced tyrosine phosphorylation in endothelial cells requires Rac1-dependent production of ROS.
- BiologyAmerican journal of physiology. Cell physiology
- 1999
The GTPase Rac1 mediates the shear-induced tyrosine phosphorylation of MAP kinase via regulation of the flow-dependent redox changes in endothelial cells in physiological and pathological circumstances.
ATP-independent membrane depolarization with ischemia in the oxygen-ventilated isolated rat lung.
- Biology, ChemistryAmerican journal of respiratory cell and molecular biology
- 1998
Results indicate that endothelial cell membrane depolarization represents an early event with lung ischemia, and postulate that membranedepolarization results from elimination of shear stress, possibly via inactivation of flow-sensitive K+-channels.
In situ imaging of intracellular calcium with ischemia in lung subpleural microvascular endothelial cells.
- Biology, MedicineAntioxidants & redox signaling
- 1999
It is concluded that increased ROS generation with 'oxygenated' lung ischemia is associated with influx of Ca2+ and an increase in endothelial cell cytosolic calcium concentration.
Increase of reactive oxygen species (ROS) in endothelial cells by shear flow and involvement of ROS in shear‐induced c‐fos expression
- BiologyJournal of cellular physiology
- 1998
It is demonstrated for the first time that shear force can modulate intracellular ROS levels and antioxidant activity in ECs and the ROS generation is involved in mediating shear‐induced c‐fos expression.
Oxidative stress activates extracellular signal-regulated kinases through Src and Ras in cultured cardiac myocytes of neonatal rats.
- BiologyThe Journal of clinical investigation
- 1997
The results suggest that Src family tyrosine kinases, Ras and Raf-1 are critical for ERK activation by hydroxyl radicals and that activation of ERKs may play an important role in protecting cardiac myocytes from apoptotic death following oxidative stress.
Intracellular generation of reactive oxygen species during nonhypoxic lung ischemia.
- Biology, MedicineThe American journal of physiology
- 1997
The results indicate that lung ischemia leads to intracellular oxidant generation that can be continuously monitored by surface fluorometry.






