Perivascular application of C-type natriuretic peptide attenuates neointimal hyperplasia in experimental vein grafts

Schachner, Thomas; Zou, Yping; Oberhuber, Alexander; Mairinger, Thomas; Tzankov, Alexandar; Laufer, Günther; Ott, Harald C.; Bonatti, Johannes

doi:10.1016/j.ejcts.2003.07.013

Cited by 30 publications

(13 citation statements)

References 27 publications

(28 reference statements)

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“…Thus, we wished to obtain insight into which NPR was involved in mediating CNP-induced inhibition of leukocyte rolling. In this regard, we used the selective NPR-C agonist (17), cANF [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] (because of the lack of availability of selective NPR-B antagonists). cANF [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] mimicked the inhibitory actions of CNP on leukocyte recruitment; although this observation only provides circumstantial evidence that CNP exerts its antileukocyte effects via this NPR, it does demonstrate that NPR-C activation is functionally important in the regulation of leukocyte-endothelial cell interactions.…”

Section: Discussionmentioning

confidence: 99%

“…CNP (0.1-1 M) was superfused for 10 min, and leukocyte flux was recorded. To investigate the involvement of the NPR-C in responses to CNP, the ability of the selective NPR-C agonist (17), cANF [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] (1 M) to inhibit leukocyte rolling was also explored.…”

Section: Assessment Of the Effect Of Cnp On Basal Leukocyte Activatiomentioning

confidence: 99%

“…When administered locally by adenoviral gene transfer, CNP inhibits neointimal hyperplasia and thrombus formation in vein grafts (13,14) and promotes vascular regeneration in models of limb ischaemia (15). Moreover, CNP expression is up-regulated in human atherosclerotic lesions (16).…”

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confidence: 99%

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C-type natriuretic peptide inhibits leukocyte recruitment and platelet-leukocyte interactions via suppression of P-selectin expression

Scotland

Cohen

Foster

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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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 ischemia͞ 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-1␤ 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 cANF 4 -23 . CNP also suppressed leukocyte rolling induced by IL-1␤ 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.endothelium ͉ natriuretic peptide receptor type C ͉ atherosclerosis ͉ thrombosis L eukocyte recruitment and platelet activation at sites of tissue injury are important facets of an inflammatory response and are pivotal in the pathogenesis of a number of cardiovascular disorders including atherosclerosis and sepsis. These processes are triggered by specific inflammatory stimuli and are critically dependent on the expression of a series of adhesion molecules on the surface of leukocytes, platelets, and the vascular endothelium (1). However, this is a dynamic process; under basal (physiological) conditions, leukocyte and platelet activation is held in check by specific endothelium-derived mediators. Perhaps the most influential of these is nitric oxide (NO), which, in concert with analogous autacoids such as prostacyclin, maintains an active suppression of leukocyte and platelet activation under physiological conditions that is paramount for maintenance of blood vessel integrity and patency (2-4).The importance of NO in the prevention of leukocyte recruitment has been established by studies demonstrating increased leukocyte-endothelial interactions in animals ...

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Section: Discussionmentioning

confidence: 99%

Section: Assessment Of the Effect Of Cnp On Basal Leukocyte Activatiomentioning

confidence: 99%

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C-type natriuretic peptide inhibits leukocyte recruitment and platelet-leukocyte interactions via suppression of P-selectin expression

Scotland

Cohen

Foster

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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“…The operation was performed as described previously [5,15,16]. In brief the vena cava from a donor mouse was interposed between two carotid artery stumps (everted over a nylon cuff) of the recipient mouse [ Fig.…”

Section: Mice and Vein Graftingmentioning

confidence: 99%

Rapamycin treatment is associated with an increased apoptosis rate in experimental vein grafts☆

Schachner

Oberhuber²,

Zou³

et al. 2005

European Journal of Cardio-Thoracic Surgery

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“…Different strategies have been proposed as adjuncts to a careful surgical technique, most of them in experimental settings. On the one hand gene therapy is a currently investigated method, and on the other hand pharmacologic interventions remain interesting options to prevent vein graft disease [5][6][7][8][9][10]. Pharmacologic treatment of vein grafts can be performed with substances that are already in clinical use and local therapy of the veins reduces the risk of side effects [6].…”

Section: Introductionmentioning

confidence: 99%

Paclitaxel treatment reduces neointimal hyperplasia in cultured human saphenous veins☆

Schachner

Steger

Heiss

et al. 2007

European Journal of Cardio-Thoracic Surgery

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Perivascular application of C-type natriuretic peptide attenuates neointimal hyperplasia in experimental vein grafts

Abstract: We conclude that perivascular application of CNP inhibits neointimal hyperplasia of vein grafts in a mouse model. These results suggest that CNP may have a therapeutic potential for the prevention of vein graft disease.

Cited by 30 publications

References 27 publications

C-type natriuretic peptide inhibits leukocyte recruitment and platelet-leukocyte interactions via suppression of P-selectin expression

C-type natriuretic peptide inhibits leukocyte recruitment and platelet-leukocyte interactions via suppression of P-selectin expression

Rapamycin treatment is associated with an increased apoptosis rate in experimental vein grafts☆

Paclitaxel treatment reduces neointimal hyperplasia in cultured human saphenous veins☆

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