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Jacqueline A Jones

Publications and source records attributed to Jacqueline A Jones.

2 recordsLinked to original sources

Surface chemistry mediates adhesive structure, cytoskeletal organization, and fusion of macrophages.

Surface chemistry modulates many critical functions of monocyte/macrophages such as adhesion, fusion, spreading, phagocytosis, and secretion. In this study, we investigated the effect of silicone modification on adhesive structure development and cytoskeletal reorganization of adherent macrophages on polyurethanes. Confocal scanning laser microscopy (CSLM) was used for qualitative and quantitative evaluation of cytoskeletal reorganization of adherent macrophages. Data presented here showed less spreading for adherent cells on silicone-modified materials due to the higher hydrophobicity and protein adsorption profile. This decrease in spreading was accompanied by less F-actin content in adherent cells on silicone-modified polyurethanes and PDMS control, indicating that silicone modification reduces the strength of adhesion. With the addition of interleukin-4 (IL-4) at days 3 and 7 to our culture, adherent cell morphology dramatically changed. The change in morphology led to higher macrophage fusion and foreign body giant cell (FBGC) formation on silicone modified materials after 10 days. In addition, mannose receptor (MR) expression was up-regulated on the silicone-modified polyurethanes and PDMS control in the presence of IL-4. Up-regulation of MR expression suggests an alternatively activated phenotype for adherent macrophages, which is accompanied with an attenuated proinflammatory cytokine production and reactive oxygen secretion. It appears that silicone modification accelerates acquisition of an alternative macrophage and FBGC phenotype, which may then result in increased polyurethane biostability.

Actins↗

Macrophage behavior on surface-modified polyurethanes.

Adherent macrophages and foreign body giant cells (FBGCs) are known to release degradative molecules that can be detrimental to the long-term biostability of polyurethanes. The modification of polyurethanes using surface modifying endgroups (SMEs) and/or the incorporation of silicone into the polyurethane soft segments may alter macrophage adhesion, fusion and apoptosis resulting in improved long-term biostability. An in vitro study of macrophage adhesion, fusion and apoptosis was performed on polyurethanes modified with fluorocarbon SMEs, polyethylene oxide (PEO) SMEs, or poly(dimethylsiloxane) (PDMS) co-soft segment and SMEs. The fluorocarbon SME and PEO SME modifications were shown to have no effect on macrophage adhesion and activity, while silicone modification had varied effects. Macrophages were capable of adapting to the surface and adhering in a similar manner to the silicone-modified and unmodified polyurethanes. In the absence of IL-4, macrophage fusion was comparable on the modified and unmodified polyurethanes, while macrophage apoptosis was promoted on the silicone modified surfaces. In contrast, when exposed to IL-4, a cytokine known to induce FBGC formation, silicone modification resulted in more macrophage fusion to form foreign body giant cells. In conclusion, fluorocarbon SME and PEO SME modification does not affect macrophage adhesion, fusion and apoptosis, while silicone modification is capable of mediating macrophage fusion and apoptosis. Silicone modification may be utilized to direct the fate of adherent macrophages towards FBGC formation or cell death through apoptosis.

Apoptosis↗