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Photodynamic therapy mediated induction of accelerated re-endothelialisation following injury to the arterial wall. Implications for the prevention of postinterventional restenosis

 
: Adili, F.; Scholz, T.; Hille, M.; Heckenkamp, J.; Barth, S.; Engert, A.; Schmitz-Rixen, T.

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European journal of vascular and endovascular surgery 24 (2002), No.2, pp.166-175
ISSN: 1078-5884
ISSN: 1532-2165
English
Journal Article
Fraunhofer IME ()
photodynamic therapy; endothelial cell; restenosis; bFGF

Abstract
Objective: accelerated re-endothelialisation may inhibit the development of restenosis. Basic Fibroblast Growth Factor (bFGF) plays a key role for early proliferative activity in the artery following injury. Therefore, this study was devised to examine the effect of photodynamic therapy (PDT) on post-injury re-endothelialisation in vivo, and bFGF-mRNA expression in endothelial cells (EC) in vitro.
Materials and methods: rat carotid arteries were balloon-injured prior to PDT. Arteries were analysed after 1, 3, 5, 14 and 30 days. Morphometric measurements were undertaken following injection of 0.5% Evans Blue which stains non-endothelialised surfaces only. To identify EC, immunohistochemistry (CD-31) was performed. Proliferation was assessed by fluorescence cell counting. PCR quantification of bFGF-mRNA expression and proliferation were assessed in bovine aortic EC which were plated on isolated, PDT-treated EC-derived extracellular matrix at (12), 24, 48 (72 h).
Results: three days following PDT, arteries displayed significantly increased endothelial lining (p = 0.02), which was more pronounced at 5 (p = 0.03) and 14 days (p = 0.02). At 30 days no relevant differences between PDT and control were noted. EC proliferation on PDT-treated matrix was significantly increased at 24, 48, and 72 h (p = 0.0004), whereas bFGF-mRNA expression was significantly increased at 24 h only (p = 0.007).
Conclusion: post-injury PDT appears to accelerate re-endothelialisation. Expression of bFGF-mRNA, however, although increased shortly after PDT, may not be responsible for a constant stimulation of EC proliferation.

: http://publica.fraunhofer.de/documents/B-79006.html