caa a22 4500 477120288 CHVBK 20180405111634.0 cr unu---uuuuu 170330e19960401xx s 000 0 eng 10.1007/BF00227904 doi (NATIONALLICENCE)springer-10.1007/BF00227904 Prevention of late lumen loss after coronary angioplasty by photodynamic therapy: Role of activated neutrophils [Elektronische Daten] [Wim Sluiter, Wil de Vree, Anneke Pietersma, Johan Koster] Restenosis after coronary angioplasty arises from fibrocellular intimal hyperplasia and possibly failure of the artery to enlarge adequately. Which mechanisms underlie this process is only partly understood. No drugs have been clinically effective in reducing the incidence of restenosis. Since recently, photodynamic therapy (PDT) is being investigated as a possible treatment for intimal hyperplasia. PDT involves the systemic administration of a light-excitable photosensitizer that is takers up rather preferentially by rapidly proliferating cells. During laser irradiation light energy is transferred from the photosensitizer to oxygen generating the highly reactive singlet oxygen. This potent oxidizer can cause severe cellular damage. After PDT of a balloon-injured artery from the rat and rabbit the media remained acellular for several weeks to months, and intimal hyperplasia did not occur. The endothelial lining regenerated by two weeks, but why smooth muscle cells did not repopulated the media is not known. Neutrophils seem to play an important role in the prevention of restenosis after coronary angioplasty, since the activation status of this type of phagocyte is directly related to vessel diameter at late follow-up. Furthermore, it has been observed that neutrophils adhere to the microvascular wall upon PDT in vivo. In vitro findings suggest that the increased neutrophil adherence was not dependent on a decreased release of the anti-adhesive factors NO and prostacyclin by the PDT-treated endothelial cells. Furthermore, PDT did not stimulate the expression of P-selectin by the endothelial cells, one of the adhesion receptors for neutrophils. The endothelial cells only retract upon PDT allowing the adherence of neutrophils by their β2-integrin adhesion receptors to the subendothelial matrix. On the basis of these findings, we presume that the successful prevention of intimal hyperplasia by PDT partly depends on the presence of the neutrophil at the site of the lesion. Kluwer Academic Publishers, 1996 coronary angioplasty nationallicence intimal hyperplasia nationallicence restenosis nationallicence smooth muscle cell nationallicence neutrophil nationallicence photodynamic therapy nationallicence Sluiter Wim Department of Biochemistry, Faculty of Medicine and Health Sciences, Erasmus University, Rotterdam, The Netherlands aut de Vree Wil Department of Biochemistry, Faculty of Medicine and Health Sciences, Erasmus University, Rotterdam, The Netherlands aut Pietersma Anneke Department of Biochemistry, Faculty of Medicine and Health Sciences, Erasmus University, Rotterdam, The Netherlands aut Koster Johan Department of Biochemistry, Faculty of Medicine and Health Sciences, Erasmus University, Rotterdam, The Netherlands aut Molecular and Cellular Biochemistry Kluwer Academic Publishers 157/1-2(1996-04-01), 233-238 0300-8177 157:1-2<233 1996 157 11010 https://doi.org/10.1007/BF00227904 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00227904 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Sluiter Wim Department of Biochemistry, Faculty of Medicine and Health Sciences, Erasmus University, Rotterdam, The Netherlands aut NATIONALLICENCE 700 1- de Vree Wil Department of Biochemistry, Faculty of Medicine and Health Sciences, Erasmus University, Rotterdam, The Netherlands aut NATIONALLICENCE 700 1- Pietersma Anneke Department of Biochemistry, Faculty of Medicine and Health Sciences, Erasmus University, Rotterdam, The Netherlands aut NATIONALLICENCE 700 1- Koster Johan Department of Biochemistry, Faculty of Medicine and Health Sciences, Erasmus University, Rotterdam, The Netherlands aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Kluwer Academic Publishers 157/1-2(1996-04-01), 233-238 0300-8177 157:1-2<233 1996 157 11010 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer