Schwarz G. Henriques, Sarah

[["dc.bibliographiccitation.firstpage","3914"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Journal of Cell Science"],["dc.bibliographiccitation.lastpage","3920"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Schwarz G. Henriques, Sarah"],["dc.contributor.author","Sandmann, Rabea"],["dc.contributor.author","Strate, Alexander"],["dc.contributor.author","Köster, Sarah"],["dc.date.accessioned","2017-09-07T11:48:27Z"],["dc.date.available","2017-09-07T11:48:27Z"],["dc.date.issued","2012"],["dc.description.abstract","Contraction at the cellular level is vital for living organisms. The most prominent type of contractile cells are heart muscle cells, a less-well-known example is blood platelets. Blood platelets activate and interlink at injured blood vessel sites, finally contracting to form a compact blood clot. They are ideal model cells to study the mechanisms of cellular contraction, as they are simple, having no nucleus, and their activation can be triggered and synchronized by the addition of thrombin. We have studied contraction using human blood platelets, employing traction force microscopy, a single-cell technique that enables time-resolved measurements of cellular forces on soft substrates with elasticities in the physiological range (similar to 4 kPa). We found that platelet contraction reaches a steady state after 25 min with total forces of similar to 34 nN. These forces are considerably larger than what was previously reported for platelets in aggregates, demonstrating the importance of a single-cell approach for studies of platelet contraction. Compared with other contractile cells, we find that platelets are unique, because force fields are nearly isotropic, with forces pointing toward the center of the cell area."],["dc.identifier.doi","10.1242/jcs.108126"],["dc.identifier.gro","3142481"],["dc.identifier.isi","000309525300022"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8762"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0021-9533"],["dc.relation.orgunit","Institut für Röntgenphysik"],["dc.relation.workinggroup","RG Köster (Cellular Biophysics)"],["dc.subject.gro","cellular biophysics"],["dc.title","Force field evolution during human blood platelet activation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2365"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","Soft Matter"],["dc.bibliographiccitation.lastpage","2371"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Sandmann, Rabea"],["dc.contributor.author","Schwarz G. Henriques, Sarah"],["dc.contributor.author","Rehfeldt, Florian"],["dc.contributor.author","Köster, Sarah"],["dc.date.accessioned","2017-09-07T11:46:55Z"],["dc.date.available","2017-09-07T11:46:55Z"],["dc.date.issued","2014"],["dc.description.abstract","Injuries in blood vessels are accompanied by disrupted endothelial cell layers. Missing or destroyed endothelial cells lead to rough, structured surfaces on the micrometer scale. The first cells to arrive at the site of injury and to cover the wound are platelets, which subsequently drive blood clot formation. Therefore, investigating the interactions of platelets with structured surfaces is essential for the understanding of blood clotting. Here, we study the effects of underlying topography on platelet spreading using microstructured model substrates with varying area fractions of protein coating. We thereby distinguish the effects of (physical) topography and of (biochemical) protein availability. By analyzing the cell area and morphology, we find that the extent of protrusion formation - but not the total spread area - is determined by the area fractions of coating. The extent of filopodia formation is influenced by the availability of binding sites and the reaction of cells to the substrate's topography. The cells react to the structured substrate by avoiding topographic holes at the cell periphery and thus adapting their outer shape. This finding leads us to the conclusion that both chemically blocked and fibrinogen-coated holes represent \"energetic obstacles\" to the cells. Thus, the shape of the cell is governed by the interplay between spreading to an optimized area and adaption to the substrate topography."],["dc.identifier.doi","10.1039/c3sm52636d"],["dc.identifier.gro","3142215"],["dc.identifier.isi","000333115900005"],["dc.identifier.pmid","24623273"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5810"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Deutsche Forschungs Gemeinschaft [SFB 937/A12]; Excellence Initiative"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1744-6848"],["dc.relation.issn","1744-683X"],["dc.relation.orgunit","Institut für Röntgenphysik"],["dc.relation.workinggroup","RG Köster (Cellular Biophysics)"],["dc.subject.gro","cellular biophysics"],["dc.title","Micro-topography influences blood platelet spreading"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]