Key result
PAR1 activation rapidly reduces distal lung transepithelial resistance without altering small-solute permeability.
Why the study?
Protease-activated receptor 1 signaling may affect lung epithelial barrier function, but its impact on bioelectric properties and permeability is unclear.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for PAR1 in distal lung epithelia; leaves open in vivo barrier effects and clinical relevance.
Proteinases contribute to the pathogenesis of various lung diseases, partly through activating cell surface receptors by limited proteolytic cleavage. The authors provide evidence that in primary cultures of distal lung epithelia, basolateral protease-activated receptor 1 activation rapidly reduces transepithelial resistance but does not alter paracellular permeability to small uncharged solutes. Changes in transepithelial resistance were partially blocked by ion transport inhibitors and were completely blocked by placing cells in low chloride buffer. In vivo studies did not reveal enhanced lung permeability in response to pulmonary or intravenous administration of protease-activated receptor 1 activators. This information is relevant as strategies to inhibit protease-activated receptor 1 signaling are considered in order to preserve lung epithelial barrier function.
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Moraes et al. (2009) studied Lung diseases. Protease-activated receptor 1 activation was evaluated on Transepithelial resistance and paracellular permeability. Protease-activated receptor 1 activation rapidly reduces transepithelial resistance in distal lung epithelia without altering paracellular permeability to small uncharged solutes.
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