Meyer, Daniel

[["dc.bibliographiccitation.artnumber","3767"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Neubert, Elsa"],["dc.contributor.author","Meyer, Daniel"],["dc.contributor.author","Rocca, Francesco"],["dc.contributor.author","Günay, Gökhan"],["dc.contributor.author","Kwaczala-Tessmann, Anja"],["dc.contributor.author","Grandke, Julia"],["dc.contributor.author","Senger-Sander, Susanne"],["dc.contributor.author","Geisler, Claudia"],["dc.contributor.author","Egner, Alexander"],["dc.contributor.author","Schön, Michael P."],["dc.contributor.author","Erpenbeck, Luise"],["dc.contributor.author","Kruss, Sebastian"],["dc.date.accessioned","2019-07-09T11:45:55Z"],["dc.date.available","2019-07-09T11:45:55Z"],["dc.date.issued","2018"],["dc.description.abstract","Neutrophilic granulocytes are able to release their own DNA as neutrophil extracellular traps (NETs) to capture and eliminate pathogens. DNA expulsion (NETosis) has also been documented for other cells and organisms, thus highlighting the evolutionary conservation of this process. Moreover, dysregulated NETosis has been implicated in many diseases, including cancer and inflammatory disorders. During NETosis, neutrophils undergo dynamic and dramatic alterations of their cellular as well as sub-cellular morphology whose biophysical basis is poorly understood. Here we investigate NETosis in real-time on the single-cell level using fluorescence and atomic force microscopy. Our results show that NETosis is highly organized into three distinct phases with a clear point of no return defined by chromatin status. Entropic chromatin swelling is the major physical driving force that causes cell morphology changes and the rupture of both nuclear envelope and plasma membrane. Through its material properties, chromatin thus directly orchestrates this complex biological process."],["dc.identifier.doi","10.1038/s41467-018-06263-5"],["dc.identifier.pmid","30218080"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15346"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59338"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2041-1723"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Chromatin swelling drives neutrophil extracellular trap release"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2320"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Gruhn, Antonia Luise"],["dc.contributor.author","Kudryasheva, Galina"],["dc.contributor.author","Günay, Gökhan"],["dc.contributor.author","Meyer, Daniel"],["dc.contributor.author","Busse, Julia"],["dc.contributor.author","Neubert, Elsa"],["dc.contributor.author","Erpenbeck, Luise"],["dc.contributor.author","Schön, Michael P."],["dc.contributor.author","Rehfeldt, Florian"],["dc.contributor.author","Kruss, Sebastian"],["dc.date.accessioned","2020-11-18T14:37:03Z"],["dc.date.available","2020-11-18T14:37:03Z"],["dc.date.issued","2019"],["dc.description.abstract","Neutrophils are the most abundant type of white blood cells. Upon stimulation, they are able to decondense and release their chromatin as neutrophil extracellular traps (NETs). This process (NETosis) is part of immune defense mechanisms but also plays an important role in many chronic and inflammatory diseases such as atherosclerosis, rheumatoid arthritis, diabetes, and cancer. For this reason, much effort has been invested into understanding biochemical signaling pathways in NETosis. However, the impact of the mechanical micro-environment and adhesion on NETosis is not well-understood. Here, we studied how adhesion and especially substrate elasticity affect NETosis. We employed polyacrylamide (PAA) gels with distinctly defined elasticities (Young's modulus E) within the physiologically relevant range from 1 to 128 kPa and coated the gels with integrin ligands (collagen I, fibrinogen). Neutrophils were cultured on these substrates and stimulated with potent inducers of NETosis: phorbol 12-myristate 13-acetate (PMA) and lipopolysaccharide (LPS). Interestingly, PMA-induced NETosis was neither affected by substrate elasticity nor by different integrin ligands. In contrast, for LPS stimulation, NETosis rates increased with increasing substrate elasticity (E > 20 kPa). LPS-induced NETosis increased with increasing cell contact area, while PMA-induced NETosis did not require adhesion at all. Furthermore, inhibition of phosphatidylinositide 3 kinase (PI3K), which is involved in adhesion signaling, completely abolished LPS-induced NETosis but only slightly decreased PMA-induced NETosis. In summary, we show that LPS-induced NETosis depends on adhesion and substrate elasticity while PMA-induced NETosis is completely independent of adhesion."],["dc.identifier.doi","10.3389/fimmu.2019.02320"],["dc.identifier.pmid","31632402"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16478"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/68803"],["dc.language.iso","en"],["dc.notes.intern","DeepGreen Import"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-3224"],["dc.relation.issn","1664-3224"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Effect of Adhesion and Substrate Elasticity on Neutrophil Extracellular Trap Formation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]