Enhancing in vivo cell and tissue targeting by modulation of polymer nanoparticles and macrophage decoys.

The in vivo efficacy of polymeric nanoparticles (NPs) is dependent on their pharmacokinetics, including time in circulation and tissue tropism. Here we explore the structure-function relationships guiding physiological fate of a library of poly(amine-co-ester) (PACE) NPs with different compositions and surface properties. We find that circulation half-life as well as tissue and cell-type tropism is dependent on polymer chemistry, vehicle characteristics, dosing, and strategic co-administration of distribution modifiers, suggesting that physiological fate can be optimized by adjusting these parameters.

Influencing Endothelial Cells' Roles in Inflammation and Wound Healing Through Nucleic Acid Delivery.

Tissue engineering and wound-healing interventions are often designed for use in diseased and inflamed environments. In this space, endothelial cells (ECs) are crucial regulators of inflammation and healing, as they are the primary contact for recruitment of immune cells, as well as production of proinflammatory cytokines, which can stimulate or reduce inflammation. Alternatively, proliferation and spreading of ECs result in the formation of new vascular tissue or repair of damaged tissue, both critical for wound healing.

Interfering with the ERC1-LL5β interaction disrupts plasma membrane-Associated platforms and affects tumor cell motility.

Cell migration requires a complex array of molecular events to promote protrusion at the front of motile cells. The scaffold protein LL5β interacts with the scaffold ERC1, and recruits it at plasma membrane-associated platforms that form at the front of migrating tumor cells. LL5 and ERC1 proteins support protrusion during migration as shown by the finding that depletion of either endogenous protein impairs tumor cell motility and invasion.