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Dive into the research topics where Timothy Scott-Burden is active.

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Featured researches published by Timothy Scott-Burden.


Biochemical and Biophysical Research Communications | 1990

Inducibleendothelin mRNA expression and peptide secretion in cultured human vascular smooth muscle cells

Thérèse J. Resink; Alfred W.A. Hahn; Timothy Scott-Burden; Jerry S. Powell; Erika Weber; Fritz R. Bühler

Abstract This study demonstrates the induction of endothelin (ET) mRNA expression and synthesis of functional ET -peptide in cultured human vascular smooth muscle cells (hVSMC). Compounds eliciting such responses in hVSMC include the vasoconstrictor hormones angiotensin II and arginine-vasopressin and the growth factors transforming growth factor s, platelet derived growth factor AA and epidermal growth factor. Induction of ET mRNA expression in hVSMC exhibited transient kinetics (peak at 3–5 hrs. and return to basal within 7 hrs.) which differed from the more sustained ET transcript induction observed for porcine endothelial cells. ET peptide (determined by both radioimmuno-and radioreceptor assays) produced by stimulated hVSMC attained levels (∼ 120–160 pg/10 6 cells/4 hrs.; concentration ∼ 3 × 10 −11 M) within the biologically effective concentration range of ET. Stimulated secretion of ET from hVSMC was abolished in the presence of the protein synthesis inhibitor cycloheximide. Sep-pak C 18 extracts of medium from stimulated hVSMC elicited a concentration-dependent phosphoinositide catabolic response in myo-[2- 3 H]-inositol-prelabelled hVSMC. Our findings invoke a role for ET which extends beyond the paracrine regulation by peptide synthesized and secreted by endothelial cells. We propose that VSMC-synthesized ET may function in an autocrine manner to regulate both tone and structural modelling of vasculature.


Circulation Research | 1992

Platelet-derived growth factor suppresses and fibroblast growth factor enhances cytokine-induced production of nitric oxide by cultured smooth muscle cells. Effects on cell proliferation.

Timothy Scott-Burden; Valérie B. Schini; E Elizondo; Didier Junquero; Paul M. Vanhoutte

Stimulation of thymidine incorporation by basic fibroblast growth factor or epidermal growth factor treatment of cultured quiescent smooth muscle cells (rat and human) was attenuated by the concomitant treatment with interleukin-1 beta in the presence of indomethacin. Platelet-derived growth factor-AB and -BB-induced thymidine incorporation was not inhibited by the presence of the cytokine under similar experimental conditions. Elevation of nitrite levels in the conditioned medium of cultures exposed to interleukin-1 beta correlated with the inhibition of thymidine incorporation. Platelet-derived growth factor-AB and -BB inhibited the production of nitric oxide (measured as nitrite levels in conditioned medium) by cells treated simultaneously with interleukin-1 beta and growth factor. However, platelet-derived growth factor-AA neither affected nitrite production nor thymidine incorporation by smooth muscle cells. Levels of cytokine-stimulated nitrite production by smooth muscle cells were increased synergistically by the presence of fibroblast growth factors or epidermal growth factor. The inhibition of thymidine incorporation and concomitant elevation of nitrite production was abolished in the presence of nitro-L-arginine. Cultures maintained in the presence of low levels of the cytokine for 9 days were growth-inhibited, and this was reversed when culture medium was supplemented with nitro-L-arginine. The treatment of smooth muscle cells, which were grown in coculture inserts with the cytokine to induce nitric oxide production, before their combination with other quiescent layers of cells resulted in the inhibition of thymidine incorporation by this second layer of cells regardless of the growth factor used for stimulation. Nitric oxide may act as an endogenous inhibitor of smooth muscle cell proliferation in the vessel wall, and impairment of its production may be one action of potent vascular mitogens such as platelet-derived growth factor.


Biochemical and Biophysical Research Communications | 1991

Interleukin-1 β induces the production of an L-arginine-derived relaxing factor from cultured smooth muscle cells from rat aorta

Valérie B. Schini; Didier Junquero; Timothy Scott-Burden; Paul M. Vanhoutte

The effect of interleukin-1 beta on the production of non-prostanoid vasoactive factors by cultured rat aortic smooth muscle cells was investigated. Under bioassay conditions, the perfusate from a column of confluent cells grown on beads and treated with interleukin-1 beta (1 ng/ml for 18 to 24 hr) abolished the contraction of a canine coronary ring without endothelium contracted by phenylephrine (1 microM), while the perfusate from control cells had no effect. The relaxing activity of the perfusate was observed when transit times were increased from 1 sec to 5 min. Nitro L-arginine (100 microM) reversed the relaxations and L-arginine stereoselectively restored the relaxations. Interleukin-1 beta (1 ng/ml) evoked a time-dependent accumulation of cyclic GMP but not cyclic AMP in cultured smooth muscle cells. The transfer of fresh or stored (-70 degrees C) conditioned culture medium from interleukin-1 beta-treated cells but not from control cells, to cultured smooth muscle cells stimulated the production of cyclic GMP. These observations demonstrate that interleukin-1 beta induces the production of transferable factor which relaxes vascular smooth muscle and stimulates the production of cyclic GMP.


The Journal of Physiology | 1992

Inhibition of cytokine-induced nitric oxide production by transforming growth factor-beta 1 in human smooth muscle cells.

Didier Junquero; Timothy Scott-Burden; Valérie B. Schini; Paul M. Vanhoutte

1. Experiments were performed to investigate the effects of human recombinant interleukin‐1 beta on the production of vasoactive substances by human aortic smooth muscle cells in culture. Smooth muscle cells were cultured either on microcarrier beads for bioassay experiments, or in multiwell plates for the determination of nitrite levels. 2. Cells were grown on microcarrier beads, treated with interleukin‐1 beta or vehicle (control) for 24 h, and packed in a column which was perfused with oxygenated Krebs‐Ringer solution in the presence of indomethacin. The activity of the perfusates was bioassayed by measuring the changes in tension of a contracted ring of Wistar rat aorta without endothelium, and by evaluating the modulation of thrombin‐induced platelet aggregation. 3. Perfusates from interleukin‐1 beta treated cells evoked relaxations of the contracted detector tissues, and microcarrier beads covered with treated cells inhibited thrombin‐induced platelet aggregation. Superoxide dismutase enhanced these effects whereas Methylene Blue abolished them. Control cells evoke neither relaxation nor inhibition of platelet aggregation. Interleukin‐1 beta induced a time‐ and concentration‐dependent production of nitrite. Cycloheximide and nitro‐L‐arginine inhibited the relaxations and the production of nitrite evoked by interleukin‐1 beta‐treated cells. L‐Arginine but not D‐arginine overcame the blockade elicited by nitro‐L‐arginine. Transforming growth factor‐beta 1 reduced the interleukin‐1 beta‐dependent generation of nitrite by cultured smooth muscle cells and relaxation of contracted bioassay tissues. 4. Interleukin‐1 beta, transforming growth factor‐beta 1, Methylene Blue and L‐arginine‐related compounds did not induce significant variations of tension of the detector rings. 5. These data demonstrate that the inflammatory and immunological mediator interleukin‐1 can stimulate the production of a nitric oxide‐like substance(s) in cultured human smooth muscle cells leading to the activation of soluble guanylate cyclase. Liberation of transforming growth factor‐beta by activated platelets may inhibit these reactions.


Biochemical Pharmacology | 1996

Regulation of interleukin-1β-stimulated inducible nitric oxide synthase expression in cultured vascular smooth muscle cells by hemostatic proteins

William Durante; Michael H. Kroll; Gregory J. Orloff; James M. Cunningham; Timothy Scott-Burden; Paul M. Vanhoutte; Andrew I. Schafer

Experiments were performed to examine the mechanism by which specific hemostatic proteins regulate the release of nitric oxide (NO) from interleukin-1 beta (IL-1beta) stimulated cultured rate aortic smooth muscle cells. Treatment of smooth muscle cells with IL-Beta stimulated inducible nitric oxide synthase (iNOS) mRNA expression, which preceded the release of NO (as measured by the accumulation of nitrite in the culture media). The cytokine-stimulated production of nitrite was blocked by the protein synthesis inhibitor cycloheximide, the transcriptional inhibitor actinomycin D, and the competitive inhibitor of NOS nitro-L-arginine. However, only actinomycin D inhibited IL-1beta-stimulated iNOS mRNA expression, Treatment of smooth muscle cells with IL-1beta in the presence of platelet derived growth factor or thrombin resulted in the inhibition of cytokine-stimulated expression of iNOS mRNA and NO release. The inhibitory effect of thrombin was reversed by hirudin and was mimicked by a 14 amino acid thrombin receptor activating peptide. In contract, the concomitant exposure of smooth muscle cells to IL-1beta-and plasmin resulted resulted in the potentiation of both IL-1beta-stimulated iNOS expression and NO generation. Finally, treatment of smooth muscle cells with IL-1beta in the presence of the hemostatic proteins did not affect the half-life of iNOS mRNA. These results demonstrate that specific protein components of the hemostatic system regulate IL- 1beta-stimulated iNOS mRNA expression in vascular smooth muscle cells. The capacity of hemostatic proteins to modulate the induction of vascular iNOS activity may play an important role in governing the release of NO and regulating thrombogenesis in vivo.


Clinical and Experimental Hypertension | 1991

Platelet-Derived Growth Factor A-Chain Homodimer Stimulated Growth of Cultured Smooth Muscle Cells from Spontaneously Hypertensive Rats

Timothy Scott-Burden; Thérèse J. Resink; Alfred A.W. Hahn; Fritz R. Bühler

Vascular smooth muscle cells from spontaneously hypertensive rats (SHR) were growth stimulated when cocultured with bovine aortic endothelial cells whereas myocytes from normotensive, Wistar Kyoto rats (WKY) were growth inhibited. The responsiveness of cells from the two rat sources to the two homodimeric forms of platelet-derived growth factor (PDGF-AA or -BB) was different; SHR-derived cells responding equally well to both PDGF forms whereas cells from WKY responded to the B-chain homodimer only. The responses measured included S6 kinase activation, phospholipase C mediated phosphoinositide catabolism and cell growth. Saturation binding experiments using [125I]-labelled PDGF homodimers (AA or BB) indicated that smooth muscle cells from hypertensive rats possess similar numbers of cell-surface A-chain receptors (alpha subunits) as Swiss 3T3 cells which have been used to characterize the mitogenic effects of the two PDGF homodimeric forms. The differences in responsiveness of SHR vs WKY cells to PDGF-AA and to the influence of endothelial cells may reside in their differential expression of PDGF receptors.


American Journal of Hypertension | 1993

Enhanced Production of Nitric Oxide in Aortae From Spontaneously Hypertensive Rats by Interleukin-1β

Didier Junquero; Valérie B. Schini; Timothy Scott-Burden; Paul M. Vanhoutte


American Journal of Physiology-heart and Circulatory Physiology | 1991

Platelet inhibition by an L-arginine-derived substance released by IL-1β-treated vascular smooth muscle cells

William Durante; V. B. Schini; Timothy Scott-Burden; D. C. Junquero; M. H. Kroll; Paul M. Vanhoutte; Andrew I. Schafer


American Journal of Hypertension | 1989

Atrial natriuretic peptide: binding and cyclic GMP response in cultured vascular smooth muscle cells from spontaneously hypertensive rats.

Thérèse J. Resink; Timothy Scott-Burden; Jones Cr; Baur U; Bühler Fr


American Journal of Physiology-heart and Circulatory Physiology | 1993

Thrombin inhibits induction of nitric oxide synthase in vascular smooth muscle cells.

V. B. Schini; S. Catovsky; William Durante; Timothy Scott-Burden; Andrew I. Schafer; Paul M. Vanhoutte

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Didier Junquero

Baylor College of Medicine

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V. B. Schini

Baylor College of Medicine

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William Durante

Baylor College of Medicine

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Fritz R. Bühler

University Hospital of Basel

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E Elizondo

Baylor College of Medicine

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