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Mechanisms of Reduced Human Vascular Cell Migration After Photodynamic Therapy ¶
Author(s) -
Waterman Peter R.,
Overhaus Marcus,
Heckenkamp Joerg,
Nigri Giuseppe R.,
Fungaloi Patrick F. C.,
Landis Michael E.,
Kossodo Sylvie C.,
LaMuraglia Glenn M.
Publication year - 2002
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1562/0031-8655(2002)0750046morhvc2.0.co2
Subject(s) - extracellular matrix , photodynamic therapy , in vivo , restenosis , intimal hyperplasia , matrix metalloproteinase , microbiology and biotechnology , cell migration , hyperplasia , chemistry , ex vivo , cancer research , cell , vascular smooth muscle , pathology , in vitro , biology , medicine , endocrinology , biochemistry , smooth muscle , organic chemistry , stent
Restenosis results from intimal hyperplasia and constrictive remodeling following cardiovascular interventions. Photodynamic therapy (PDT) has been shown to inhibit intimal hyperplasia in vivo by preventing neointimal repopulation of the treated vessel. This study was undertaken in an attempt to further dissect the mechanisms by which PDT acts on secreted and extracellular matrix proteins to inhibit migration of cultured human vascular cells. PDT of three‐dimensional collagen gels inhibited invasive human smooth muscle cell (SMC) migration, whereas cell‐derived matrix metalloproteinase production remained unaltered. Additionally, PDT generated cross‐links in the collagen gels, a result substantiated in an ex vivo model whereby PDT rendered the treated vessels resistant to pepsin digestion and inhibited invasive migration of SMC and fibroblasts. These data support the premise that by inducing matrix protein cross‐links, rendering the vessel resistant to degradation, in vivo PDT inhibits repopulation of the vessel and therefore intimal hyperplasia.