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Research Service, Stratton Veterans Affairs Medical Center; and the Center for Cardiovascular Science, The Albany Medical College, Albany, New York 12208
The intracellular
serine/threonine kinase protein kinase C (PKC) has an important role in
the genesis of pulmonary edema. This review discusses the PKC-mediated
mechanisms that participate in the pulmonary endothelial response to
agents involved in lung injury characteristic of the respiratory
distress syndrome. Thus the paradigms of PKC-induced lung injury are
discussed within the context of pulmonary transvascular fluid exchange.
We focus on the signal transduction pathways that are modulated by PKC and their effect on lung endothelial permeability. Specifically, 
-thrombin, tumor necrosis factor (TNF)-, and reactive oxygen species are discussed because of their well-established roles in both
human and experimental lung injury. We conclude that PKC, most likely
PKC-, is a primary supporter for lung endothelial injury in response
to -thrombin, TNF-, and reactive oxygen species.
antisense; edema; reactive oxygen species; transcription
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