The Obituary of Ivalon Arterial Grafts

Fitch, Edward; Denman, Frank R.; Waldron, George W.

doi:10.1001/archsurg.1960.01300050146026

Cited by 16 publications

(1 citation statement)

References 8 publications

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“…We have shown that the absence of PECAM-1 can attenuate neovascularization, extracellular matrix deposition and leukocyte accumulation in and around these sterile, inert PVA implants. Although PVA sponges have been retired from their use as human arterial grafts, 46 they are widely used to study cellular components of foreign body reaction: angiogenesis, granuloma formation, and extracellular matrix deposition. 45,47,48 It will be of great interest to pursue potential clinical applications of this finding, including the use of local PECAM-1-blocking reagents (anti-sense oligonucleotides, PECAM-1 antibodies, recombinant PECAM-1 peptides) coupled to synthetic prosthetic devices or local delivery of such reagents to the site(s) of prosthetic implants to ameliorate the fibrotic complications that result in functional compromise of prosthetic devices including cardiac and vascular patches and arteriovenous shunt prosthetics.…”

Section: Discussionmentioning

confidence: 99%

Lack of Platelet Endothelial Cell Adhesion Molecule-1 Attenuates Foreign Body Inflammation because of Decreased Angiogenesis

Solowiej¹,

Biswas²,

Graesser³

et al. 2003

The American Journal of Pathology

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Platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31) is a 130-kd member of the immunoglobulin superfamily of proteins, expressed on endothelial cells, leukocytes, and platelets. Antibody-blocking studies have implicated it in modulating leukocyte transmigration and angiogenesis. However, the generation of the PECAM-1 knockout mouse has shown that its function can be compensated for by similarly acting proteins because most acute inflammatory models proceed in a comparable manner in wild-type and knockout animals. We decided to examine the function of PECAM-1 in the chronic process of foreign body inflammation. We show that PECAM-1-deficient mice exhibit attenuated neutrophil infiltration in and around a subcutaneous polyvinyl acetyl implant. Bone marrow engraftment studies indicate that the lack of CD31 expression on the endothelium determines the diminished leukocyte accumulation in the knockout implants. Specifically, we find that decreased angiogenesis (as manifested by lower vessel density, decreased hemoglobin content, and less laminin deposition) correlates with lower neutrophil accumulation in the knockout animals. This study indicates that the absence of endothelial PECAM-1 results in decreased angiogenesis and therefore in diminished delivery of leukocytes to the foreign body implants.

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Section: Discussionmentioning

confidence: 99%