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- W36595162 abstract "In the lung, several endothelial cell (EC) processes are regulated by an increase in EC cytosolic Ca2+. However, the role of EC cytosolic Ca2+ in mediating capillary proinflammatory processes is not clear. Mainly, it is not clear to what extent EC cytosolic Ca2+ increases activate other second messengers, which in turn might play a direct role in initiating proinflammatory responses. We determined this in intact lung capillaries using videomicroscopy and image analysis. We subjected the lungs to stressors including increased vascular pressure and tumor necrosis factor α. Our studies indicate that the primary response to these lung stresses is an increase in EC cytosolic Ca2+. These stresses induce proinflammatory responses in these capillaries, as indicated by the increase in P-selectin expression. However, determination of the signaling pathways underlying the Ca2+-induced P-selectin expression indicates a role for mitochondrial mechanisms. The lung stressors induce cytosolic Ca2+-dependent increases in mitochondrial Ca2+ and reactive oxygen species, which in turn regulate exocytosis of P-selectin. Hence, mitochondrial reactive oxygen species act as signaling intermediates in Ca2+-induced P-selectin exocytosis in lung capillaries. Thus, second messengers Ca2+ and mitochondrial reactive oxygen species are critical in the regulation of lung proinflammatory responses." @default.
- W36595162 created "2016-06-24" @default.
- W36595162 creator A5053962419 @default.
- W36595162 date "2005-01-01" @default.
- W36595162 modified "2023-10-16" @default.
- W36595162 title "Second-Messenger Signaling in Lung Capillaries" @default.
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- W36595162 doi "https://doi.org/10.1007/978-1-59259-909-7_15" @default.
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