Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 284, Issue 3, Pages L435-L451Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00106.2002
Keywords
antisense; edema; reactive oxygen species; transcription
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Funding
- NHLBI NIH HHS [HL-59901-02] Funding Source: Medline
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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, alpha-thrombin, tumor necrosis factor (TNF)-alpha, 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-alpha, is a primary supporter for lung endothelial injury in response to alpha-thrombin, TNF-alpha, and reactive oxygen species.
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