Phospholipids in the cell membranes of all eukaryotic cells contain phosphatidyl choline (PC) as the headgroup. Here we show that hyperbranched polyglycerols (HPGs) decorated with the 'PC-inverse' choline phosphate (CP) in a polyvalent fashion can electrostatically bind to a variety of cell membranes and to PC-containing liposomes, the binding strength depending on the number density of CP groups per macromolecule. We also show that HPG-CPs can cause cells to adhere with varying affinity to other cells, and that binding can be reversed by subsequent exposure to low molecular weight HPGs carrying small numbers of PCs. Moreover, PC-rich membranes adsorb and rapidly internalize fluorescent HPG-CP but not HPG-PC molecules, which suggests that HPG-CPs could be used as drug-delivery agents. CP-decorated polymers should find broad use, for instance as tissue sealants and in the self-assembly of lipid nanostructures.
Migration of dendritic cells (DCs) into tissues and secondary lymphoid organs plays a crucial role in the initiation of innate and adaptive immunity. In this article, we show that cyclosporin A (CsA) impairs the migration of DCs both in vitro and in vivo. Exposure of DCs to clinical concentrations of CsA neither induces apoptosis nor alters development but does impair cytokine secretion, chemokine receptor expression, and migration. In vitro, CsA impairs the migration of mouse bone marrow–derived DCs toward macrophage inflammatory protein-3β (MIP-3β) and induces them to retain responsiveness to MIP-1α after lipopolysaccharide (LPS)–stimulated DC maturation, while in vivo administration of CsA inhibits the migration of DCs out of skin and into the secondary lymphoid organs. CsA impairs chemokine receptor and cyclooxygenase-2 (COX-2) expression normally triggered in LPS-stimulated DCs; administration of exogenous prostaglandin E2 (PGE2) reverses the effects of CsA on chemokine receptor expression and DC migration. Inhibition of nuclear factor–κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathway signaling by CsA may be responsible for the CsA-mediated effects on the regulation of chemokine receptor and cyclooxygenase-2 (COX-2) expression. Impairment of DC migration due to inhibition of PGE2 production and regulation of chemokine receptor expression may contribute, in part, to CsA-mediated immunosuppression.
Polyaniline
is one of the most investigated conducting polymers
as supercapacitor material for energy storage applications. The preparation
of nanostructured polyaniline with well-controlled morphology is crucial
to obtaining good supercapacitor performance. We present here a facile
chemical process to produce polyaniline nanostructures with three
different morphologies (i.e., nanofibers, nanospheres, and nanotubes)
by utilizing the corresponding tunable morphology of MnO2 reactive templates. A growth mechanism is proposed to explain the
evolution of polyaniline morphology based on the reactive templates.
The morphology-induced improvement in the electrochemical performance
of polyaniline pseudocapacitors is as large as 51% due to the much
enhanced surface area and the porous nature of the template-guided
polyaniline nanostructures. In addition, and for the first time, a
redox-active electrolyte is applied to the polyaniline pseudocapacitors
to achieve significant enhancement of pseudocapacitance. Compared
to the conventional electrolyte, the enhancement of pseudocapacitance
in the redox-active electrolyte is 49%–78%, depending on the
specific polyaniline morphology, reaching the highest reported capacitance
of 896 F/g for polyaniline full cells so far.
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