The urea decomposition product cyanate promotes endothelial dysfunction
The dramatic cardiovascular mortality of patients with chronic kidney disease is attributable in a significant proportion to endothelial dysfunction. Cyanate, a reactive species in equilibrium with urea, is formed in excess in chronic kidney disease. Cyanate is thought to have a causal role in promo...
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| Veröffentlicht in: | Kidney international 2014-11, Vol.86 (5), p.923-931 |
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| creator | El-Gamal, Dalia Rao, Shailaja P. Holzer, Michael Hallström, Seth Haybaeck, Johannes Gauster, Martin Wadsack, Christian Kozina, Andrijana Frank, Saša Schicho, Rudolf Schuligoi, Rufina Heinemann, Akos Marsche, Gunther |
| description | The dramatic cardiovascular mortality of patients with chronic kidney disease is attributable in a significant proportion to endothelial dysfunction. Cyanate, a reactive species in equilibrium with urea, is formed in excess in chronic kidney disease. Cyanate is thought to have a causal role in promoting cardiovascular disease, but the underlying mechanisms remain unclear. Immunohistochemical analysis performed in the present study revealed that carbamylated epitopes associate mainly with endothelial cells in human atherosclerotic lesions. Cyanate treatment of human coronary artery endothelial cells reduced expression of endothelial nitric oxide synthase, and increased tissue factor and plasminogen activator inhibitor-1 expression. In mice, administration of cyanate, promoting protein carbamylation at levels observed in uremic patients, attenuated arterial vasorelaxation of aortic rings in response to acetylcholine without affecting the sodium nitroprusside–induced relaxation. Total endothelial nitric oxide synthase and nitric oxide production were significantly reduced in aortic tissue of cyanate-treated mice. This coincided with a marked increase of tissue factor and plasminogen activator inhibitor-1 protein levels in aortas of cyanate-treated mice. Thus, cyanate compromises endothelial functionality in vitro and in vivo. This may contribute to the dramatic cardiovascular risk of patients suffering from chronic kidney disease. |
| doi_str_mv | 10.1038/ki.2014.218 |
| format | Article |
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Cyanate, a reactive species in equilibrium with urea, is formed in excess in chronic kidney disease. Cyanate is thought to have a causal role in promoting cardiovascular disease, but the underlying mechanisms remain unclear. Immunohistochemical analysis performed in the present study revealed that carbamylated epitopes associate mainly with endothelial cells in human atherosclerotic lesions. Cyanate treatment of human coronary artery endothelial cells reduced expression of endothelial nitric oxide synthase, and increased tissue factor and plasminogen activator inhibitor-1 expression. In mice, administration of cyanate, promoting protein carbamylation at levels observed in uremic patients, attenuated arterial vasorelaxation of aortic rings in response to acetylcholine without affecting the sodium nitroprusside–induced relaxation. Total endothelial nitric oxide synthase and nitric oxide production were significantly reduced in aortic tissue of cyanate-treated mice. This coincided with a marked increase of tissue factor and plasminogen activator inhibitor-1 protein levels in aortas of cyanate-treated mice. Thus, cyanate compromises endothelial functionality in vitro and in vivo. This may contribute to the dramatic cardiovascular risk of patients suffering from chronic kidney disease.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/ki.2014.218</identifier><identifier>PMID: 24940796</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Administration, Inhalation ; Animals ; Aorta - drug effects ; Aorta - metabolism ; Aorta - physiopathology ; Cells, Cultured ; Citrulline - analogs & derivatives ; Citrulline - metabolism ; cyanate ; Cyanates - administration & dosage ; Cyanates - pharmacology ; Dose-Response Relationship, Drug ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; endothelial nitric oxide synthase ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - physiopathology ; Humans ; Male ; Mice, Inbred C57BL ; Nitric Oxide Synthase Type III - genetics ; Nitric Oxide Synthase Type III - metabolism ; Phenotype ; Plasminogen Activator Inhibitor 1 - genetics ; Plasminogen Activator Inhibitor 1 - metabolism ; plasminogen activator inhibitor-1 ; Protein Processing, Post-Translational ; renal disease ; RNA, Messenger - metabolism ; Thromboplastin - metabolism ; Time Factors ; tissue factor ; Vasodilation - drug effects ; Vasodilator Agents - pharmacology</subject><ispartof>Kidney international, 2014-11, Vol.86 (5), p.923-931</ispartof><rights>2014 International Society of Nephrology</rights><rights>Copyright Nature Publishing Group Nov 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-ae84c8323fbc512aee344423e69522072095cf34bd7f09fb1ea5734aec35b1e53</citedby><cites>FETCH-LOGICAL-c525t-ae84c8323fbc512aee344423e69522072095cf34bd7f09fb1ea5734aec35b1e53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1618912547?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>230,314,780,784,885,27923,27924,64384,64388,72240</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24940796$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>El-Gamal, Dalia</creatorcontrib><creatorcontrib>Rao, Shailaja P.</creatorcontrib><creatorcontrib>Holzer, Michael</creatorcontrib><creatorcontrib>Hallström, Seth</creatorcontrib><creatorcontrib>Haybaeck, Johannes</creatorcontrib><creatorcontrib>Gauster, Martin</creatorcontrib><creatorcontrib>Wadsack, Christian</creatorcontrib><creatorcontrib>Kozina, Andrijana</creatorcontrib><creatorcontrib>Frank, Saša</creatorcontrib><creatorcontrib>Schicho, Rudolf</creatorcontrib><creatorcontrib>Schuligoi, Rufina</creatorcontrib><creatorcontrib>Heinemann, Akos</creatorcontrib><creatorcontrib>Marsche, Gunther</creatorcontrib><title>The urea decomposition product cyanate promotes endothelial dysfunction</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>The dramatic cardiovascular mortality of patients with chronic kidney disease is attributable in a significant proportion to endothelial dysfunction. Cyanate, a reactive species in equilibrium with urea, is formed in excess in chronic kidney disease. Cyanate is thought to have a causal role in promoting cardiovascular disease, but the underlying mechanisms remain unclear. Immunohistochemical analysis performed in the present study revealed that carbamylated epitopes associate mainly with endothelial cells in human atherosclerotic lesions. Cyanate treatment of human coronary artery endothelial cells reduced expression of endothelial nitric oxide synthase, and increased tissue factor and plasminogen activator inhibitor-1 expression. In mice, administration of cyanate, promoting protein carbamylation at levels observed in uremic patients, attenuated arterial vasorelaxation of aortic rings in response to acetylcholine without affecting the sodium nitroprusside–induced relaxation. Total endothelial nitric oxide synthase and nitric oxide production were significantly reduced in aortic tissue of cyanate-treated mice. This coincided with a marked increase of tissue factor and plasminogen activator inhibitor-1 protein levels in aortas of cyanate-treated mice. Thus, cyanate compromises endothelial functionality in vitro and in vivo. This may contribute to the dramatic cardiovascular risk of patients suffering from chronic kidney disease.</description><subject>Administration, Inhalation</subject><subject>Animals</subject><subject>Aorta - drug effects</subject><subject>Aorta - metabolism</subject><subject>Aorta - physiopathology</subject><subject>Cells, Cultured</subject><subject>Citrulline - analogs & derivatives</subject><subject>Citrulline - metabolism</subject><subject>cyanate</subject><subject>Cyanates - administration & dosage</subject><subject>Cyanates - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>endothelial nitric oxide synthase</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Humans</subject><subject>Male</subject><subject>Mice, Inbred C57BL</subject><subject>Nitric Oxide Synthase Type III - 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Cyanate, a reactive species in equilibrium with urea, is formed in excess in chronic kidney disease. Cyanate is thought to have a causal role in promoting cardiovascular disease, but the underlying mechanisms remain unclear. Immunohistochemical analysis performed in the present study revealed that carbamylated epitopes associate mainly with endothelial cells in human atherosclerotic lesions. Cyanate treatment of human coronary artery endothelial cells reduced expression of endothelial nitric oxide synthase, and increased tissue factor and plasminogen activator inhibitor-1 expression. In mice, administration of cyanate, promoting protein carbamylation at levels observed in uremic patients, attenuated arterial vasorelaxation of aortic rings in response to acetylcholine without affecting the sodium nitroprusside–induced relaxation. Total endothelial nitric oxide synthase and nitric oxide production were significantly reduced in aortic tissue of cyanate-treated mice. This coincided with a marked increase of tissue factor and plasminogen activator inhibitor-1 protein levels in aortas of cyanate-treated mice. Thus, cyanate compromises endothelial functionality in vitro and in vivo. This may contribute to the dramatic cardiovascular risk of patients suffering from chronic kidney disease.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>24940796</pmid><doi>10.1038/ki.2014.218</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Administration, Inhalation Animals Aorta - drug effects Aorta - metabolism Aorta - physiopathology Cells, Cultured Citrulline - analogs & derivatives Citrulline - metabolism cyanate Cyanates - administration & dosage Cyanates - pharmacology Dose-Response Relationship, Drug Endothelial Cells - drug effects Endothelial Cells - metabolism endothelial nitric oxide synthase Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Endothelium, Vascular - physiopathology Humans Male Mice, Inbred C57BL Nitric Oxide Synthase Type III - genetics Nitric Oxide Synthase Type III - metabolism Phenotype Plasminogen Activator Inhibitor 1 - genetics Plasminogen Activator Inhibitor 1 - metabolism plasminogen activator inhibitor-1 Protein Processing, Post-Translational renal disease RNA, Messenger - metabolism Thromboplastin - metabolism Time Factors tissue factor Vasodilation - drug effects Vasodilator Agents - pharmacology |
| title | The urea decomposition product cyanate promotes endothelial dysfunction |
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