Complementary targeting of liposomes to IL-1? and TNF-? activated endothelial cells via the transient expression of VCAM1 and E-selectin
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https://doi.org/10.1016/j.biomaterials.2011.08.093Metadata
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Gunawan, Rico C., Dariela Almeda, and Debra T. Auguste. 2011. “Complementary Targeting of Liposomes to IL-1? and TNF-? Activated Endothelial Cells via the Transient Expression of VCAM1 and E-Selectin.” Biomaterials 32 (36) (December): 9848–9853. doi:10.1016/j.biomaterials.2011.08.093.Abstract
Inflammation is in part defined by the transient upregulation of cell adhesion molecules on the surface of endothelial cells (ECs) in response to cytokines. We hypothesized that liposomes with a complementary surface presentation of antibodies to the pattern of molecules on the EC surface may enhance targeting. We quantified the expression of vascular cell adhesion molecule-1 (VCAM1) and endothelial leukocyte cell adhesion molecule-1 (E-selectin) on ECs upon exposure to either tumor necrosis factor-α (TNF-α) or interleukin-1α (IL-1α) as a function of time. Liposomes, composed of 95 mol% dioleoyl phosphatidylcholine (DOPC) and 5 mol% dodecanyl phosphatidylethanolamine (N-dod-PE), were prepared by conjugating different molar ratios of antibodies against VCAM1 (aVCAM1) and E-selectin (aE-selectin). Increased binding was observed when immunoliposomes complemented the presentation of VCAM1:E-selectin expressed on TNF-α activated ECs. The 1:1 aVCAM1:aE-selectin liposomes had maximal binding at both 6 and 24 h on IL-1α activated ECs due to differences in molecular organization. The results demonstrate that liposomes targeting to inflamed endothelium may be optimized by exploiting the dynamic expression of VCAM1 and E-selectin on the EC surface.Terms of Use
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