Showing papers by "Elena E. Pohl published in 2006"
TL;DR: Trypsin and tryptase as well as specific agonists for PAR2 were able to induce Ca2+ mobilization in HPMCs, and agonists of PAR2 induce the release of histamine from these cells, indicating a role ofPAR2 in regulating inflammatory and immune responses by skin mast cells.
111 citations
TL;DR: An automated technique for reconstitution of membrane proteins into lipid bilayer membranes is described, which substantially reduces both the reconstitutes time and the amount of protein required for the membrane formation.
34 citations
TL;DR: The data indicate that MAF is expressed in selected macrophages/microglial cells around the lesion and in the degenerating hippocampus after ECL, and MAF expression in monocytic cells seems to play a functional role in the differentiation to a phagocytosing phenotype and may be, at least partially, required for phagocytes activity, specifically in lesioned tissue after brain trauma.
Abstract: After traumatic brain lesion, microglial cells are rapidly activated, migrate toward the sites of injury, and cause secondary damage that accounts for most of the loss of brain function. In the present study, we have characterized a new macrophage/microglia activation factor (MAF). Using the monocytic cell line U937, we were able to demonstrate that MAF is upregulated after TPA-induced differentiation into macrophages. We have generated a specific antibody against MAF. In BV-2 microglial cells, MAF is partially co-localized with IB4, a classical microglial marker. In addition, we have analyzed the in vivo expression patterns of MAF after entorhinal cortex lesion. We were able to show a substantial upregulation of MAF on selected CD11b(+) and IB4(+) macrophages/microglial cells in the deafferented hippocampus and in the perilesional region, while no MAF expression was detectable on the contralateral side. Confocal microscopy revealed a lysosome-like expression pattern in BV-2 cells, as well as in ECL-associated macrophages/microglial cells in vivo. Furthermore, we were able to demonstrate that U937 cells with downregulated MAF converted slower and to a significantly reduced extent to the macrophageal phenotype after TPA treatment. In addition, MAF downregulation in BV-2 microglial cells substantially reduced the phagocytotic uptake of dextran beads. Our data indicate that MAF is expressed in selected macrophages/microglial cells around the lesion and in the degenerating hippocampus after ECL. Furthermore, MAF expression in monocytic cells seems to play a functional role in the differentiation to a phagocytosing phenotype and may be, at least partially, required for phagocytotic activity, specifically in lesioned tissue after brain trauma.
24 citations
Patent•
07 Apr 2006TL;DR: In this paper, a method for forming a lipid bilayer membrane is provided, the method comprising forming a layer (22) of lipid molecules on a liquid surface at an air-liquid interface between a liquid volume and an air volume.
Abstract: A method for forming a lipid bilayer membrane is provided, the method comprising forming a layer (22) of lipid molecules on a liquid surface at an air-liquid interface between a liquid volume and an air volume. An aperture is moved from the liquid volume to the air volume through the layer (22) of lipid molecules to form a lipid monolayer membrane (23) at the aperture, the aperture being at an end of bilayer former (3). The aperture is then moved from the air volume to the liquid volume through the layer (22) of lipid molecules to form the bilayer membrane (21). An angle of >90° is maintained between the liquid surface and a surface (20) of the aperture during the formation of the lipid monolayer membrane (23) and during the formation of the lipid bilayer membrane (21).
9 citations