C-Type Natriuretic Peptide Inhibits Leukocyte Recruitment and Platelet-Leukocyte Interactions via Suppression of P-Selectin Expression
The multifaceted process of immune cell recruitment to sites of tissue injury is key to the development of an inflammatory response and involved in the pathogenesis of numerous cardiovascular disorders. We recently identified C-type natriuretic peptide (CNP) as an important endothelium-derived media...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2005-10, Vol.102 (40), p.14452-14457 |
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| creator | Scotland, Ramona S. Cohen, Marc Foster, Paul Lovell, Matthew Mathur, Anthony Ahluwalia, Amrita Hobbs, Adrian J. Moncada, Salvador |
| description | The multifaceted process of immune cell recruitment to sites of tissue injury is key to the development of an inflammatory response and involved in the pathogenesis of numerous cardiovascular disorders. We recently identified C-type natriuretic peptide (CNP) as an important endothelium-derived mediator that regulates vascular tone and protects against myocardial ischemia/reperfusion injury. Herein, we investigated whether CNP inhibits leukocyte recruitment and platelet aggregation and thereby exerts a potential antiinflammatory influence on the blood vessel wall. We assessed the effects of CNP on leukocyte-endothelial cell interactions in mouse mesenteric postcapillary venules in vivo in animals with high basal leukocyte activation (endothelial nitric oxide synthase knockout mice, eNOS-/-) or under acute inflammatory conditions (induced by interleukin-1β or histamine). CNP suppressed basal leukocyte rolling in eNOS-/-mice in a rapid, reversible, and concentration-dependent manner. These effects of CNP were mimicked by the selective natriuretic peptide receptor-C agonist cANF4-23. CNP also suppressed leukocyte rolling induced by IL-1β or histamine, inhibited platelet-leukocyte interactions, and prevented thrombin-induced platelet aggregation of human blood. Furthermore, analysis of human umbilical vein endothelial cells, leukocytes, and platelets revealed that CNP selectively attenuates expression of P-selectin. Thus, CNP is a modulator of acute inflammation in the blood vessel wall characterized by leukocyte and platelet activation. These antiinflammatory effects appear to be mediated, at least in part, via suppression of P-selectin expression. These observations suggest that endothelial CNP might maintain an anti-atherogenic influence on the blood vessel wall and represent a target for therapeutic intervention in inflammatory cardiovascular disorders. |
| doi_str_mv | 10.1073/pnas.0504961102 |
| format | Article |
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We recently identified C-type natriuretic peptide (CNP) as an important endothelium-derived mediator that regulates vascular tone and protects against myocardial ischemia/reperfusion injury. Herein, we investigated whether CNP inhibits leukocyte recruitment and platelet aggregation and thereby exerts a potential antiinflammatory influence on the blood vessel wall. We assessed the effects of CNP on leukocyte-endothelial cell interactions in mouse mesenteric postcapillary venules in vivo in animals with high basal leukocyte activation (endothelial nitric oxide synthase knockout mice, eNOS-/-) or under acute inflammatory conditions (induced by interleukin-1β or histamine). CNP suppressed basal leukocyte rolling in eNOS-/-mice in a rapid, reversible, and concentration-dependent manner. These effects of CNP were mimicked by the selective natriuretic peptide receptor-C agonist cANF4-23. CNP also suppressed leukocyte rolling induced by IL-1β or histamine, inhibited platelet-leukocyte interactions, and prevented thrombin-induced platelet aggregation of human blood. Furthermore, analysis of human umbilical vein endothelial cells, leukocytes, and platelets revealed that CNP selectively attenuates expression of P-selectin. Thus, CNP is a modulator of acute inflammation in the blood vessel wall characterized by leukocyte and platelet activation. These antiinflammatory effects appear to be mediated, at least in part, via suppression of P-selectin expression. These observations suggest that endothelial CNP might maintain an anti-atherogenic influence on the blood vessel wall and represent a target for therapeutic intervention in inflammatory cardiovascular disorders.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0504961102</identifier><identifier>PMID: 16179391</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Analysis of Variance ; Animals ; Atrial Natriuretic Factor - pharmacology ; Biological Sciences ; Blood ; Blood vessels ; Cardiovascular disease ; Endothelial cells ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - physiology ; Flow Cytometry ; Gene Expression Regulation - drug effects ; Histamines ; Humans ; Immune system ; Inflammation - metabolism ; Leukocytes ; Leukocytes - drug effects ; Leukocytes - metabolism ; Mice ; Mice, Knockout ; Molecules ; Natriuretic Peptide, C-Type - agonists ; Natriuretic Peptide, C-Type - metabolism ; Natriuretic Peptide, C-Type - pharmacology ; Natriuretic peptides ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type III ; P-Selectin - metabolism ; Peptide Fragments - pharmacology ; Peptides ; Platelet aggregation ; Platelet Aggregation - drug effects ; Platelet Aggregation - physiology ; Platelets ; Venules ; Venules - cytology</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2005-10, Vol.102 (40), p.14452-14457</ispartof><rights>Copyright 1993/2005 The National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Oct 4, 2005</rights><rights>Copyright © 2005, The National Academy of Sciences 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c595t-36aea9cd13d38fbe536899842216cee0e5bae232aac1db23692899f0a8ccb7453</citedby><cites>FETCH-LOGICAL-c595t-36aea9cd13d38fbe536899842216cee0e5bae232aac1db23692899f0a8ccb7453</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/102/40.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3376759$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3376759$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16179391$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Scotland, Ramona S.</creatorcontrib><creatorcontrib>Cohen, Marc</creatorcontrib><creatorcontrib>Foster, Paul</creatorcontrib><creatorcontrib>Lovell, Matthew</creatorcontrib><creatorcontrib>Mathur, Anthony</creatorcontrib><creatorcontrib>Ahluwalia, Amrita</creatorcontrib><creatorcontrib>Hobbs, Adrian J.</creatorcontrib><creatorcontrib>Moncada, Salvador</creatorcontrib><title>C-Type Natriuretic Peptide Inhibits Leukocyte Recruitment and Platelet-Leukocyte Interactions via Suppression of P-Selectin Expression</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>The multifaceted process of immune cell recruitment to sites of tissue injury is key to the development of an inflammatory response and involved in the pathogenesis of numerous cardiovascular disorders. We recently identified C-type natriuretic peptide (CNP) as an important endothelium-derived mediator that regulates vascular tone and protects against myocardial ischemia/reperfusion injury. Herein, we investigated whether CNP inhibits leukocyte recruitment and platelet aggregation and thereby exerts a potential antiinflammatory influence on the blood vessel wall. We assessed the effects of CNP on leukocyte-endothelial cell interactions in mouse mesenteric postcapillary venules in vivo in animals with high basal leukocyte activation (endothelial nitric oxide synthase knockout mice, eNOS-/-) or under acute inflammatory conditions (induced by interleukin-1β or histamine). CNP suppressed basal leukocyte rolling in eNOS-/-mice in a rapid, reversible, and concentration-dependent manner. These effects of CNP were mimicked by the selective natriuretic peptide receptor-C agonist cANF4-23. CNP also suppressed leukocyte rolling induced by IL-1β or histamine, inhibited platelet-leukocyte interactions, and prevented thrombin-induced platelet aggregation of human blood. Furthermore, analysis of human umbilical vein endothelial cells, leukocytes, and platelets revealed that CNP selectively attenuates expression of P-selectin. Thus, CNP is a modulator of acute inflammation in the blood vessel wall characterized by leukocyte and platelet activation. These antiinflammatory effects appear to be mediated, at least in part, via suppression of P-selectin expression. These observations suggest that endothelial CNP might maintain an anti-atherogenic influence on the blood vessel wall and represent a target for therapeutic intervention in inflammatory cardiovascular disorders.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Atrial Natriuretic Factor - pharmacology</subject><subject>Biological Sciences</subject><subject>Blood</subject><subject>Blood vessels</subject><subject>Cardiovascular disease</subject><subject>Endothelial cells</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - physiology</subject><subject>Flow Cytometry</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Histamines</subject><subject>Humans</subject><subject>Immune system</subject><subject>Inflammation - metabolism</subject><subject>Leukocytes</subject><subject>Leukocytes - drug effects</subject><subject>Leukocytes - metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Molecules</subject><subject>Natriuretic Peptide, C-Type - agonists</subject><subject>Natriuretic Peptide, C-Type - metabolism</subject><subject>Natriuretic Peptide, C-Type - pharmacology</subject><subject>Natriuretic peptides</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type III</subject><subject>P-Selectin - metabolism</subject><subject>Peptide Fragments - pharmacology</subject><subject>Peptides</subject><subject>Platelet aggregation</subject><subject>Platelet Aggregation - drug effects</subject><subject>Platelet Aggregation - physiology</subject><subject>Platelets</subject><subject>Venules</subject><subject>Venules - cytology</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk9vEzEQxS0EoqFw5oKQxQGJw7b-s95dX5BQVCBSBBEtZ8vrnaUOG3tre6vmC_C5cZTQAJeeLPn93vPMeBB6SckZJTU_H52OZ0SQUlaUEvYIzSiRtKhKSR6jGSGsLpqSlSfoWYxrQogUDXmKTmhFa8klnaFf8-JqOwL-olOwU4BkDV7BmGwHeOGubWtTxEuYfnqzTYC_gQmTTRtwCWvX4dWgEwyQiiOycAmCNsl6F_Gt1fhyGscAMeYL7Hu8Ki6zI-sOX9z9EZ6jJ70eIrw4nKfo-8eLq_nnYvn102L-YVkYIUUqeKVBS9NR3vGmb0HwqpEyd8hoZQAIiFYD40xrQ7uW8UqyrPdEN8a0dSn4KXq_zx2ndgOdyX0EPagx2I0OW-W1Vf8qzl6rH_5WUVYyTmgOeHsICP5mgpjUxkYDw6Ad-CmqqqlqQenDIK25lEI0GXzzH7j2U3B5CorlBxtOyQ4630Mm-BgD9PclU6J2m6B2m6COm5Adr__u9Mgfvj4D-ADsnMc4psocWZZil_HuAUT10zAkuEuZfbVn1zH5cA9zXueBSP4baK7UkA</recordid><startdate>20051004</startdate><enddate>20051004</enddate><creator>Scotland, Ramona S.</creator><creator>Cohen, Marc</creator><creator>Foster, Paul</creator><creator>Lovell, Matthew</creator><creator>Mathur, Anthony</creator><creator>Ahluwalia, Amrita</creator><creator>Hobbs, Adrian J.</creator><creator>Moncada, Salvador</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20051004</creationdate><title>C-Type Natriuretic Peptide Inhibits Leukocyte Recruitment and Platelet-Leukocyte Interactions via Suppression of P-Selectin Expression</title><author>Scotland, Ramona S. ; 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We recently identified C-type natriuretic peptide (CNP) as an important endothelium-derived mediator that regulates vascular tone and protects against myocardial ischemia/reperfusion injury. Herein, we investigated whether CNP inhibits leukocyte recruitment and platelet aggregation and thereby exerts a potential antiinflammatory influence on the blood vessel wall. We assessed the effects of CNP on leukocyte-endothelial cell interactions in mouse mesenteric postcapillary venules in vivo in animals with high basal leukocyte activation (endothelial nitric oxide synthase knockout mice, eNOS-/-) or under acute inflammatory conditions (induced by interleukin-1β or histamine). CNP suppressed basal leukocyte rolling in eNOS-/-mice in a rapid, reversible, and concentration-dependent manner. These effects of CNP were mimicked by the selective natriuretic peptide receptor-C agonist cANF4-23. CNP also suppressed leukocyte rolling induced by IL-1β or histamine, inhibited platelet-leukocyte interactions, and prevented thrombin-induced platelet aggregation of human blood. Furthermore, analysis of human umbilical vein endothelial cells, leukocytes, and platelets revealed that CNP selectively attenuates expression of P-selectin. Thus, CNP is a modulator of acute inflammation in the blood vessel wall characterized by leukocyte and platelet activation. These antiinflammatory effects appear to be mediated, at least in part, via suppression of P-selectin expression. These observations suggest that endothelial CNP might maintain an anti-atherogenic influence on the blood vessel wall and represent a target for therapeutic intervention in inflammatory cardiovascular disorders.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>16179391</pmid><doi>10.1073/pnas.0504961102</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis of Variance Animals Atrial Natriuretic Factor - pharmacology Biological Sciences Blood Blood vessels Cardiovascular disease Endothelial cells Endothelium, Vascular - metabolism Endothelium, Vascular - physiology Flow Cytometry Gene Expression Regulation - drug effects Histamines Humans Immune system Inflammation - metabolism Leukocytes Leukocytes - drug effects Leukocytes - metabolism Mice Mice, Knockout Molecules Natriuretic Peptide, C-Type - agonists Natriuretic Peptide, C-Type - metabolism Natriuretic Peptide, C-Type - pharmacology Natriuretic peptides Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type III P-Selectin - metabolism Peptide Fragments - pharmacology Peptides Platelet aggregation Platelet Aggregation - drug effects Platelet Aggregation - physiology Platelets Venules Venules - cytology |
| title | C-Type Natriuretic Peptide Inhibits Leukocyte Recruitment and Platelet-Leukocyte Interactions via Suppression of P-Selectin Expression |
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