European Journal of Pharmacology

2001

DOI: 10.1016/s0014-2999(01)01336-x

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Effect of trapidil on effector functions of monocytes related to atherosclerotic plaque

¹

,

Toshihiko Tsuda

²

,

Yoshitaka Hosaka

³

et al.

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Protective Effect Of Trapidil and L-arginine 9651

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Cited by 4 publications

(8 citation statements)

References 21 publications

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“…12 The obtained results showed that trapidil significantly decreased the levels of serum, IL-1b, TNF-a, and MCP-1. These results are in accordance with the finding of Kato et al 41 Deguchi et al 42 suggested that this antiplatelet agent inhibits TNF-induced tissue factor expression on monocytes and may have a potent therapeutic value in patients with hypercoagulable state for its inhibitory property on the procoagulant activity of endothelial cells and monocytes.…”

Section: Protective Effect Of Trapidil and L-arginine 965supporting

confidence: 92%

Protective effect of trapidil andl-arginine against renal and hepatic toxicity induced by cyclosporine in rats

¹

,

²

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³

et al. 2010

Renal Failure

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(2010) Protective effect of trapidil and l-arginine against renal and hepatic toxicity induced by cyclosporine in rats, Renal Failure, 32:8,[959][960][961][962][963][964][965][966][967][968] DOI: 10.3109 CsA induced renal and hepatic dysfunction, which was confirmed by laboratory and histopathological examination. Administration of trapidil diminished the renal and liver injury and significantly attenuated the levels of serum creatinine, urea, aspartate aminotransferase (AST), alanine aminotransferase (ALT), interleukin1b (IL-1b), tumor necrosis factor alpha (TNF-a), monocyte chemoattractant protein-1 (MCP-1), and oxidative stress, while it significantly elevated the level of serum nitric oxide and the activity of antioxidative stress. L-Arginine gave the same trend as trapidil, but trapidil effect was more pronounced. Coadministration of trapidil + L-arginine significantly ameliorated the toxic effect of CsA, but did not differ significantly from the effect of trapidil alone. Conclusions: Treatment with trapidil or L-arginine diminished the renal and hepatic CsA-induced toxicity. However, the effect of trapidil was more pronounced. Therefore, treatment with trapidil alone may be the most economic and effective as a potential therapeutic agent in CsA injury.

“…12 The obtained results showed that trapidil significantly decreased the levels of serum, IL-1b, TNF-a, and MCP-1. These results are in accordance with the finding of Kato et al 41 Deguchi et al 42 suggested that this antiplatelet agent inhibits TNF-induced tissue factor expression on monocytes and may have a potent therapeutic value in patients with hypercoagulable state for its inhibitory property on the procoagulant activity of endothelial cells and monocytes.…”

Section: Protective Effect Of Trapidil and L-arginine 965supporting

confidence: 92%

Protective effect of trapidil andl-arginine against renal and hepatic toxicity induced by cyclosporine in rats

¹

,

²

,

³

et al. 2010

Renal Failure

View full text Add to dashboard Cite

(2010) Protective effect of trapidil and l-arginine against renal and hepatic toxicity induced by cyclosporine in rats, Renal Failure, 32:8,[959][960][961][962][963][964][965][966][967][968] DOI: 10.3109 CsA induced renal and hepatic dysfunction, which was confirmed by laboratory and histopathological examination. Administration of trapidil diminished the renal and liver injury and significantly attenuated the levels of serum creatinine, urea, aspartate aminotransferase (AST), alanine aminotransferase (ALT), interleukin1b (IL-1b), tumor necrosis factor alpha (TNF-a), monocyte chemoattractant protein-1 (MCP-1), and oxidative stress, while it significantly elevated the level of serum nitric oxide and the activity of antioxidative stress. L-Arginine gave the same trend as trapidil, but trapidil effect was more pronounced. Coadministration of trapidil + L-arginine significantly ameliorated the toxic effect of CsA, but did not differ significantly from the effect of trapidil alone. Conclusions: Treatment with trapidil or L-arginine diminished the renal and hepatic CsA-induced toxicity. However, the effect of trapidil was more pronounced. Therefore, treatment with trapidil alone may be the most economic and effective as a potential therapeutic agent in CsA injury.

“…Involvement of the CD40/CD40L pathway in regulating MEG-01 cell MMP-9 content was demonstrated since antibodies that blocked either CD40L or CD40 also effectively prevented enhancement of MMP-9 activity. The role of CD40L/CD40 in up-regulating MMPs is supported by the observation that trapidil, inhibitor of IFN-α-induced CD40 expression, suppresses the in vitro expression of MMPs in abdominal aortic aneurysm tissues (53)(54)(55) and that CD40-deficient macrophages displayed a reduced gelatinolytic activity (56).…”

Section: Discussionmentioning

confidence: 96%

Platelet soluble CD40L and matrix metalloproteinase 9 activity are proinflammatory mediators in Behçet disease patients

López‐Longo³

et al. 2012

Thromb Haemost

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Platelets are the major source of plasma-soluble CD40L (sCD40L), an important inflammatory mediator. This study explored the impact of platelet-derived sCD40L on Behçet disease (BD), an autoinflammatory vasculitis. We also searched for influences by platelet matrix metalloproteinases (MMP) -2 and MMP-9, implicated in several inflammatory diseases, on CD40L shedding from platelet membrane. Platelet activation were studied by flow cytometry and aggregometry, surface expression of CD40L and platelet-leukocyte aggregates by flow cytometry, sCD40L by ELISA, cellular CD40L and CD40 levels by Western blot and MMPs activity by gelatin zymography. The effect of sCD40L on MMP9 expression was studied in cultured MEG-01 cells. Plasma and platelet-released sCD40L levels were higher in BD patients. No differences in platelet activation and in platelet-leukocyte aggregates formation were observed between BD patients and controls. Plasma and platelet MMP-9 levels were increased in BD patients, whereas there was no difference in platelet MMP-2 activity. Since a correlation between plasma sCD40L and platelet MMP-9 activity was observed, we studied the influence of sCD40L on MMP-9 levels in the megakaryoblastic cell line MEG-01. Treatment of MEG-01 cells with recombinant sCD40L increased MMP-9 but did not change MMP-2 levels. In conclusion, sCD40L release from platelets was mediated by MMP-9, and MMP-9 expression was in turn upregulated by sCD40L in the MEG-01 cell line. We conclude that platelets and megakaryocytes might participate in a positive feedback loop occurring between sCD40L and MMP-9 which would contribute to the proinflammatory state observed in BD.

“…It has been reported that THP-1 cells express a variety of cell surface molecules other than B7 family proteins, such as CD40, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 [29, 30], suggesting that interaction between these molecules and counter-receptors on T cells may also play an important role in IL-5 gene transcription. In agreement with our findings, Larche et al [31]and Jaffer et al [32]reported that anti-CD86 mAb and cytotoxic T lymphocyte antigen 4-Ig fusion protein, which inhibit CD28-mediated signaling, markedly suppressed allergen-induced IL-5 production by PBMC of asthmatic patients, whereas partial responses (10–50%) remained.…”

Section: Resultsmentioning

confidence: 99%

Interaction with Monocytes Enhances IL-5 Gene Transcription in Peripheral T Cells of Asthmatic Patients

¹

,

et al. 2003

Int Arch Allergy Immunol

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Background: The regulatory mechanisms of IL-5 gene transcription in human peripheral T cells are unclear because the transfection efficiency of plasmid constructs into nontransformed T cells is very low. Methods: Concanavalin A (ConA)-stimulated blastocytes derived from peripheral blood lymphocytes of asthmatic subjects were transiently transfected with the human IL-5 gene promoter/enhancer-luciferase gene construct, pIL-5 (–511)Luc, and cultured with THP-1 cells (human monocytoid cells) and anti-CD3 monoclonal antibody (mAb). IL-5 level in the culture medium was determined by an enzyme-linked immunosorbent assay. Transcriptional activity of the IL-5 gene was measured by luciferase reporter analysis. Results: ConA-blast lymphocytes of asthmatic patients produced a significant amount of IL-5 upon combined stimulation with anti-CD3 mAb and THP-1 cells, but not with anti-CD3 mAb alone. Costimulation with anti-CD28 mAb also enhanced the anti-CD3 mAb- induced IL-5 production. Accordingly, luciferase activity induced by anti-CD3 mAb stimulation in pIL-5(–511)Luc-transfected ConA-blast lymphocytes was increased 1.9- and 3.4-fold by the addition of anti-CD28 mAb and THP-1 cells, respectively. Serial 5′ deletion analysis of the reporter gene demonstrated that the cis-regulatory element located at –119 to –80 is critical for anti-CD3 mAb-induced IL-5 gene transcription. Conclusions: Our present findings provide a useful model reflecting IL-5 gene transcription in human peripheral T cells in vivo, and clearly demonstrate that an interaction with monocytes enhances IL-5 gene transcription.

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