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  • hypoxia  (1)
  • intimal hyperplasia  (1)
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  • 1
    ISSN: 1573-4919
    Keywords: coronary angioplasty ; intimal hyperplasia ; restenosis ; smooth muscle cell ; neutrophil ; photodynamic therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract 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.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 116 (1992), S. 197-202 
    ISSN: 1573-4919
    Keywords: granulocytes ; hypoxia ; adherence ; CD11/CD18
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Granulytes play an important role in increasing the infarct size after ischemia and reperfusion by the release of oxygen-derived free radicals (ODFR) and lysosomal enzymes. It has been shown that the number of granulocytes adhering to the vascular endothelium increases after occlusion of the coronary artery, and that the area of myocardial damage can be reduced by preventing granulocyte adherence with monoclonal antibodies directed against adhesion receptors. The underlying mechanism of granulocyte activation under these conditions is not yet known. We have investigated whether granulocytes can be activated directly by reduced oxygen tensions. Granulocytes were suspended in a hypoxic buffer and incubated on fibronectin and gelatin coated microtitre plates at 1–3% ambient oxygen to study their ability to adhere to these matrices. The results showed that the adherence of granulocytes to fibronectin was dependent on the duration of hypoxia. After 30 min of incubation under hypoxia granulocyte adherence increased 1.3 to 1.8 fold compared to the normoxic control. The adherence to fibronectin could be inhibited partially by anti-CD18 antibody, a monoclonal antibody to the common beta chain of a class of extracellular matrix receptors. This direct activation of granulocytes due to hypoxic conditions may have implications for the interaction of these cells with the vascular endotheliumin vivo, (Mol Cell Biochem116: 197–202, 1992)
    Type of Medium: Electronic Resource
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