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R. C. Werthmann, M. J. Lohse and M. Bünemann Temporally resolved cAMP monitoring in endothelial cells uncovers a thrombin-induced [cAMP] elevation mediated via the Ca2+-dependent production of prostacyclin The Journal of Physiology 589

Article first published online: 23 DEC 2010 | DOI: 10.1113/jphysiol.2010.200121

Endothelial cells form the innermost layer of blood vessels and build a barrier between blood and tissue. The permeability of this barrier is antagonistically controlled by the intracellular signalling molecules Ca2+ and cAMP. A rise in Ca2+ concentration increases permeability, whereas increased cAMP levels strengthen the endothelial cell barrier. In this study we investigated the impact of the coagulation factor thrombin that is known to increase Ca2+ concentrations and endothelial permeability, on cAMP levels. Surprisingly we detected that thrombin also led to a delayed and slow increase of cAMP concentrations. We discovered that this increase is due to the production of prostacyclin and a subsequent stimulation of endothelial prostacyclin receptors that finally induce cAMP production. This thrombin-mediated increase of cAMP levels might constitute a negative feedback control to protect endothelial barrier function despite a rise of Ca2+ concentrations.

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