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  • Title: Systemic application of anti-ICAM-1 monoclonal antibodies to prevent restenosis in rabbits: an anti-inflammatory strategy.
    Author: Kollum M, Hoefer I, Schreiber R, Bode C, Hehrlein C.
    Journal: Coron Artery Dis; 2007 Mar; 18(2):117-23. PubMed ID: 17301603.
    Abstract:
    OBJECTIVES: After vascular intervention, cell adhesion molecules such as ICAM-1 and VCAM are fundamental in inflammatory processes. In particular, ICAM-1 expression is strongly associated with macrophage-rich areas in restenotic lesions. Therefore, we hypothesized an anti-restenotic effect by systemic application of anti-ICAM-1 monoclonal antibodies (mAb). METHODS: Thirty two rabbits underwent balloon angioplasty and stent implantation either in the right or left iliac artery, Animals received either anti-ICAM mAb or saline solution as a control. Animals were sacrificed 7 (n=8) and 14 (n=8) days and tissue was analyzed for basic fibroblast growth factor (bFGF) and transforming growth factor beta (TGF-beta) expression. Sixteen animals were sacrificed 6 months following treatment and tissue was harvested for histomorphometric analysis. RESULTS: After balloon injury, bFGF significantly increased from 7 to 14 days only in the control group and was significantly higher compared to the anti-ICAM group. At 14 days after stent implantation, controls showed a significant increase of both bFGF and TGF-beta, whereas the anti-ICAM group only showed a significant increase of TGF-beta. Histomorphometric analysis for neointimal growth did not show any differences between control and anti-ICAM groups either after balloon injury or after stent implantation at 6 months. CONCLUSION: Administration of anti-ICAM-1 mAb following either balloon angioplasty or stent implantation results in a suppression of bFGF in the early phase of restenosis, whereas TGF-beta significantly increases from 7 to 14 days after stent implantation independent of anti-ICAM-1 mAb application. Therefore we conclude that anti-inflammatory strategies are able to interfere with growth factor expression after vascular injury.
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