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Cardiovascular Research 2001 50(1):125-136; doi:10.1016/S0008-6363(01)00199-7
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

TGFβ is active, and correlates with activators of TGFβ, following porcine coronary angioplasty

Janet Chamberlaina,*, Julian Gunna, Sheila E. Francisa, Cathy M. Holta, Nadine D. Arnolda, David C. Cumberlanda, Mark W.J. Fergusonb and David C. Crossmana

aCardiovascular Research Group, Section of Medicine, University of Sheffield, Clinical Sciences Centre, Northern General Hospital, Herries Road, Sheffield, S5 7AU, UK
bSchool of Biological Sciences, University of Manchester, Manchester, UK

* Corresponding author. Tel.: +44-114-271-4004; fax: +44-114-261-9587 j.chamberlain{at}sheffield.ac.uk

Objective: Restenosis following angioplasty involves processes that may be influenced by local production of cytokines. We investigated the expression of active and total transforming growth factor β (TGFβ) following porcine coronary angioplasty (PTCA), and have correlated this with the expression of potential in vivo activators of TGFβ: mannose-6-phosphate/insulin-like growth factor-II (M6P/IGF-II) receptor and thrombospondin-1. Methods: Oversized porcine PTCA was performed and the arteries excised after selected intervals. Levels of in situ active and total (active plus latent) TGFβ were determined using a modified plasminogen activator–inhibitor/luciferase bioassay. Results: Levels of active TGFβ significantly increased 2 h to 7 days after angioplasty, compared to non-injured controls. Levels returned to baseline by 28 days. Active TGFβ in tissues adjacent to the injured artery did not change. Total TGFβ was significantly higher than controls 2–6 h after injury. M6P/IGF-II receptor mRNA was upregulated between 6 h and 3 days after injury, with protein detectable at 3–28 days. Thrombospondin-1 was detected between 1 h and 14 days. Conclusions: We conclude that balloon injury causes an early rapid increase in levels of active TGFβ, that correlates with the expression of TGFβ activators. Thus, TGFβ is a good potential target for anti-restenotic therapies.

KEYWORDS Angioplasty; Arteries; Growth factors; Cytokines; Restenosis


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