Meyer, Daniel

[["dc.bibliographiccitation.firstpage","9104-9115"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Nanoscale"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Meyer, Daniel"],["dc.contributor.author","Telele, Saba"],["dc.contributor.author","Zelená, Anna"],["dc.contributor.author","Gillen, Alice J."],["dc.contributor.author","Antonucci, Alessandra"],["dc.contributor.author","Neubert, Elsa"],["dc.contributor.author","Nißler, Robert"],["dc.contributor.author","Mann, Florian A."],["dc.contributor.author","Erpenbeck, Luise"],["dc.contributor.author","Boghossian, Ardemis A."],["dc.contributor.author","Köster, Sarah"],["dc.contributor.author","Kruss, Sebastian"],["dc.date.accessioned","2020-06-26T11:13:39Z"],["dc.date.available","2020-06-26T11:13:39Z"],["dc.date.issued","2020"],["dc.description.abstract","Cells can take up nanoscale materials, which has important implications for understanding cellular functions, biocompatibility as well as biomedical applications. Controlled uptake, transport and triggered release of nanoscale cargo is one of the great challenges in biomedical applications of nanomaterials. Here, we study how human immune cells (neutrophilic granulocytes, neutrophils) take up nanomaterials and program them to release this cargo after a certain time period. For this purpose, we let neutrophils phagocytose DNA-functionalized single-walled carbon nanotubes (SWCNTs) in vitro that fluoresce in the near infrared (980 nm) and serve as sensors for small molecules. Cells still migrate, follow chemical gradients and respond to inflammatory signals after uptake of the cargo. To program release, we make use of neutrophil extracellular trap formation (NETosis), a novel cell death mechanism that leads to chromatin swelling, subsequent rupture of the cellular membrane and release of the cell's whole content. By using the process of NETosis, we can program the time point of cargo release via the initial concentration of stimuli such as phorbol 12-myristate-13-acetate (PMA) or lipopolysaccharide (LPS). At intermediate stimulation, cells continue to migrate, follow gradients and surface cues for around 30 minutes and up to several hundred micrometers until they stop and release the SWCNTs. The transported and released SWCNT sensors are still functional as shown by subsequent detection of the neurotransmitter dopamine and reactive oxygen species (H2O2). In summary, we hijack a biological process (NETosis) and demonstrate how neutrophils transport and release functional nanomaterials."],["dc.identifier.doi","10.1039/d0nr00864h"],["dc.identifier.pmid","32286598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66755"],["dc.language.iso","en"],["dc.relation.eissn","2040-3372"],["dc.relation.orgunit","Institut für Röntgenphysik"],["dc.relation.workinggroup","RG Köster (Cellular Biophysics)"],["dc.rights","CC BY 3.0"],["dc.subject.gro","cellular biophysics"],["dc.title","Transport and programmed release of nanoscale cargo from cells by using NETosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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"]]