FK409, a new nitric-oxide donor, suppresses smooth muscle proliferation in the rat model of balloon angioplasty

Seki, Jiro; Nishio, Mie; Kato, Yasuko; Motoyama, Yukio; Yoshida, Keizo

doi:10.1016/0021-9150(95)05563-c

Cited by 65 publications

(40 citation statements)

References 34 publications

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“…For example, inhibiting endogenous production of NO enhances smooth muscle growth in response to injury (162). By comparison, exogenously supplied NO, either by an NO donor or inhalation, inhibits smooth muscle growth after mechanical injury (76,104,164).…”

Section: Evolving Neonatal Cld Leads To Increased Hydrostatic Pulmonamentioning

confidence: 99%

Utility of large-animal models of BPD: chronically ventilated preterm lambs

Albertine

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Albertine KH. Utility of large-animal models of BPD: chronically ventilated preterm lambs. Am J Physiol Lung Cell Mol Physiol 308: L983-L1001, 2015. First published March 13, 2015; doi:10.1152/ajplung.00178.2014.-This paper is focused on unique insights provided by the preterm lamb physiological model of bronchopulmonary dysplasia (BPD). Connections are also made to insights provided by the former preterm baboon model of BPD, as well as to rodent models of lung injury to the immature, postnatal lung. The preterm lamb and baboon models recapitulate the clinical setting of preterm birth and respiratory failure that require prolonged ventilation support for days or weeks with oxygen-rich gas. An advantage of the preterm lamb model is the large size of preterm lambs, which facilitates physiological studies for days or weeks during the evolution of neonatal chronic lung disease (CLD). To this advantage is linked an integrated array of morphological, biochemical, and molecular analyses that are identifying the role of individual genes in the pathogenesis of neonatal CLD. Results indicate that the mode of ventilation, invasive mechanical ventilation vs. less invasive high-frequency nasal ventilation, is related to outcomes. Our approach also includes pharmacological interventions that test causality of specific molecular players, such as vitamin A supplementation in the pathogenesis of neonatal CLD. The new insights that are being gained from our preterm lamb model may have important translational implications about the pathogenesis and treatment of BPD in preterm human infants.neonatal chronic lung disease; alveolarization; alveolar simplification; pulmonary hypertension; airway expiratory resistance; nitric oxide; vitamin A; endothelial nitric oxide synthase; nasal CPAP; insulin-like growth factor-1; epigenetics ACUTE RESPIRATORY FAILURE of preterm human infants reflects immaturity of the lung following preterm birth, disrupted developmental processes, and dysregulated repair responses. This reflection occurs in the neonatal intensive care setting of continuous invasive mechanical ventilation support with oxygen-rich gas that is necessary to keep many preterm human infants alive. Among survivors of preterm birth and initial days of ventilation support with oxygen-rich gas, human infants who require prolonged invasive ventilation support with oxygen-rich gas frequently develop bronchopulmonary dysplasia (BPD). BPD is a significant pediatric health problem because, almost four decades after its initial description (134), this disease of preterm infants remains the most common cause of long-term pour outcomes, including postnatal growth failure, recurrent hospitalization for respiratory tract infections, and intraventricular hemorrhage (53, 178). In the United States, since 2006, the overall rate of prematurity is 1 in 8 births, or ϳ12% (74, 118). However, the underlying pathogenic mechanisms are incompletely understood.Gaps in knowledge about the underlying pathogenic mechanisms that contribute to BPD are related, in p...

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Section: Evolving Neonatal Cld Leads To Increased Hydrostatic Pulmonamentioning

confidence: 99%

Utility of large-animal models of BPD: chronically ventilated preterm lambs

Albertine

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Local or systemic administration of NO donors and transfer of genes encoding NOS attenuate vascular injury through sGC activation. 5,6 Interestingly, gene transfer of the individual sGC subunits, sGC ␣1 and ␤1, further increase NO responsiveness in vascular injury models. 7 New NO-independent pharmacologic activators of sGC, such as BAY41-2272 and BAY 58-2667, also have a remarkable ability to stimulate sGC and thus to selectively dilate blood vessels.…”

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confidence: 99%

Vascular biology and pathobiology of the liver: Report of a single-topic symposium

2008

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Portal hypertension and its complications account for the majority of morbidity and mortality that occurs in patients with cirrhosis. In addition to portal hypertension, a number of other vascular syndromes are also of great importance, especially the ischemia-reperfusion (IR) injury. With the identification of major vascular defects that could account for many of the clinical sequelae of these syndromes, the liver vasculature field has now integrated very closely with the broader vascular biology discipline. In that spirit, the Vascular Cell Signaling Mediated by NO. Endothelial cells (ECs) produce NO through the enzyme endothelial NO synthase (eNOS). NO then regulates important vascular functions, such as vascular tone, angiogenesis, and arterial remodeling. 1 eNOS is regulated in a multiprotein complex (Fig. 1), which includes the activating kinase, Akt1 and putative negative regulator caveolin-1 (Cav-1). Although eNOS Ϫ/Ϫ mice evidence impaired angiogenesis, overexpression of a constitutively active allele of eNOS that mimics the phosphorylated and active state rescues these angiogenic defects. 2 Because eNOS is an EC-specific Akt substrate, ECs from mice lacking the Akt1 isoform also have defects in eNOS phosphorylation, NO production, and angiogenesis which are correspondingly rescued by Akt1 overexpression. 3 One key mechanism by which the Akt-eNOS axis promotes angiogenesis in vivo is through mobilization of endothelial progenitor cells and EC migration to sites of vascular injury. In contradistinction to AKT, Cav-1 is a negative regulator of eNOS. Mice deficient in Cav-1 have defective mechanotransduction, calcium signaling, prostacyclin production, and elevated NO production indicating that endothelial Cav-1 also importantly regulates vascular function by regulating eNOS and other signaling pathways. 4 Upon its generation in ECs, NO also acts on adjacent vascular effector cells to modulate vascular tone, cellular proliferation, apoptosis, migration, and synthesis of extracellular matrix (Fig. 2). NO acts in part by stimulating soluble guanylate cyclase (sGC) to produce intracellular Abbreviations: Cav-

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“…In addition to regulating vascular tone, atrial natriuretic factor (ANF), C-type natriuretic peptide (CNP), and nitric oxide-generating compounds inhibit VSMC growth and migration in vitro [27][28][29][30] and reduce neointimal formation after balloon catheter-induced vascular injury. 31,32 Nitric oxide has also been shown to provide antithrombotic activity [33][34][35] and reduce PAI-1 released from platelets. 36,37 As such, exogenous local delivery of nitric oxide synthase and CNP has been proposed as a treatment to reduce restenosis.…”

mentioning

confidence: 99%

Natriuretic Factors and Nitric Oxide Suppress Plasminogen Activator Inhibitor-1 Expression in Vascular Smooth Muscle Cells

Bouchie

Hansen

Feener

1998

ATVB

105

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Abstract-Increased expression of plasminogen activator inhibitor-1 (PAI-1) has been reported in atherosclerotic and balloon-injured vessels. Little is known regarding the factors and mechanisms that may negatively regulate PAI-1 expression. In this report, the effect of cGMP-coupled vasoactive hormones, including natriuretic factors and nitric oxide, on the regulation of PAI-1 expression in vascular smooth muscle cells was examined. Atrial natriuretic factor 1-28 (ANF) and C-type natriuretic factor-22 (CNP) reduced angiotensin II (Ang II)-and platelet-derived growth factor-stimulated PAI-1 mRNA expression in rat aortic smooth muscle cells by 50% to 70%, with corresponding reductions in PAI-1 protein release. Treatment of human aortic smooth muscle cells with CNP similarly inhibited both platelet-derived growth factor-induced PAI-1 mRNA expression and PAI-1 protein release by 50%. Dose-response studies revealed that the inhibitory effects of CNP and ANF on PAI-1 expression were concentration dependent, with IC 50 s of Ϸ1 nmol/L for both natriuretic peptides. Ang II-stimulated PAI-1 expression was also inhibited by the nitric oxide donor S-nitroso-N-acetylpenicillamine.

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FK409, a new nitric-oxide donor, suppresses smooth muscle proliferation in the rat model of balloon angioplasty

Cited by 65 publications

References 34 publications

Utility of large-animal models of BPD: chronically ventilated preterm lambs

Utility of large-animal models of BPD: chronically ventilated preterm lambs

Vascular biology and pathobiology of the liver: Report of a single-topic symposium

Natriuretic Factors and Nitric Oxide Suppress Plasminogen Activator Inhibitor-1 Expression in Vascular Smooth Muscle Cells

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