Ontology type: schema:ScholarlyArticle Open Access: True
2015-12
AUTHORSRobrecht Thoonen, Anje Cauwels, Kelly Decaluwe, Sandra Geschka, Robert E. Tainsh, Joris Delanghe, Tino Hochepied, Lode De Cauwer, Elke Rogge, Sofie Voet, Patrick Sips, Richard H. Karas, Kenneth D. Bloch, Marnik Vuylsteke, Johannes-Peter Stasch, Johan Van de Voorde, Emmanuel S. Buys, Peter Brouckaert
ABSTRACTOxidative stress, a central mediator of cardiovascular disease, results in loss of the prosthetic haem group of soluble guanylate cyclase (sGC), preventing its activation by nitric oxide (NO). Here we introduce Apo-sGC mice expressing haem-free sGC. Apo-sGC mice are viable and develop hypertension. The haemodynamic effects of NO are abolished, but those of the sGC activator cinaciguat are enhanced in apo-sGC mice, suggesting that the effects of NO on smooth muscle relaxation, blood pressure regulation and inhibition of platelet aggregation require sGC activation by NO. Tumour necrosis factor (TNF)-induced hypotension and mortality are preserved in apo-sGC mice, indicating that pathways other than sGC signalling mediate the cardiovascular collapse in shock. Apo-sGC mice allow for differentiation between sGC-dependent and -independent NO effects and between haem-dependent and -independent sGC effects. Apo-sGC mice represent a unique experimental platform to study the in vivo consequences of sGC oxidation and the therapeutic potential of sGC activators. More... »
PAGES8482
http://scigraph.springernature.com/pub.10.1038/ncomms9482
DOIhttp://dx.doi.org/10.1038/ncomms9482
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PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/26442659
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