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Neutrophil‐mediated biodegradation of medical implant materials
Author(s) -
Labow Rosalind S.,
Meek Erin,
Santerre J. Paul
Publication year - 2001
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/1097-4652(200101)186:1<95::aid-jcp1008>3.0.co;2-0
Subject(s) - biodegradation , chemistry , biochemistry , phospholipase a2 , hydrolysis , enzyme , phorbol , arachidonic acid , cell culture , viability assay , in vitro , protein kinase c , biology , organic chemistry , genetics
During the acute inflammatory response to implanted medical devices, human neutrophils (PMN) release oxidative and hydrolytic activities which may ultimately contribute to the degradation of the biomaterial. In this study, the biological activities secreted by live PMNs which may contribute to biodegradation were investigated using a 14 C label in the monomer unit of a poly(ester‐urea‐urethane) (PEUU) substrate. By using specific inhibitors, it was possible to propose a mechanism for PMN‐mediated biodegradation. PMN, labeled with 3 H‐arachidonic acid, released significantly more 3 H when adherent to PEUU than when adherent to tissue culture grade polystyrene ( P < 0.05). The phospholipase A 2 (PLA 2 ) inhibitors, aristolochic acid (ARIST) and quinacrine (QUIN), decreased the release of 3 H and inhibited PEUU biodegradation (> 50%, P < 0.05). ARIST had no effect on cell viability, whereas QUIN significantly decreased it. The serine protease inhibitor, phenylmethylsulfonylfluoride inhibited biodegradation, but did not decrease cell survival. There is evidence to suggest that activation via the PLA 2 pathway caused the release of hydrolytic activities which were able to elicit 14 C release from PEUU. The role of oxidative compounds which were released via activation by phorbol myristate acetate (PMA), was not apparent, since PMA inhibited biodegradation and cell survival (> 40%, P < 0.05). This study has shown that it is possible to find out the differences in PMN activation through the PLA 2 pathway when exposed to different material surfaces, making this a model system worthy of further investigation. J. Cell. Physiol. 186:95–103, 2001. © 2001 Wiley‐Liss, Inc.