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    PLoS One. 2010 Mar 22;5(3):e9800.

    Role of TGF-beta1 and MAP kinases in the antiproliferative effect of aspirin in human vascular smooth muscle cells.

    Redondo S, Ruiz E, Gordillo-Moscoso A, Navarro-Dorado J, Ramajo M, Carnero M, Reguillo F, Rodriguez E, Tejerina T.

    Source

    Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid, Spain.

    Abstract

    BACKGROUND:

    We aimed to test the antiproliferative effect of acetylsalicylic acid (ASA) on vascular smooth muscle cells (VSMC) from bypass surgery patients and the role of transforming growth factor beta 1 (TGF-beta1).

    METHODOLOGY/PRINCIPAL FINDINGS:

    VSMC were isolated from remaining internal mammary artery from patients who underwent bypass surgery. Cell proliferation and DNA fragmentation were assessed by ELISA. Protein expression was assessed by Western blot. ASA inhibited BrdU incorporation at 2 mM. Anti-TGF-beta1 was able to reverse this effect. ASA (2 mM) induced TGF-beta1 secretion; however it was unable to induce Smad activation. ASA increased p38(MAPK) phosphorylation in a TGF-beta1-independent manner. Anti-CD105 (endoglin) was unable to reverse the antiproliferative effect of ASA. Pre-surgical serum levels of TGF-beta1 in patients who took at antiplatelet doses ASA were assessed by ELISA and remained unchanged.

    CONCLUSIONS/SIGNIFICANCE:

    In vitro antiproliferative effects of aspirin (at antiinflammatory concentration) on human VSMC obtained from bypass patients are mediated by TGF-beta1 and p38(MAPK). Pre-surgical serum levels of TGF- beta1 from bypass patients who took aspirin at antiplatelet doses did not change.

    PMID:
    20339548
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC2842433
    Free PMC Article

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