Pietuch, Anna

[["dc.bibliographiccitation.artnumber","e80068"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Schneider, David"],["dc.contributor.author","Baronsky, Thilo"],["dc.contributor.author","Pietuch, Anna"],["dc.contributor.author","Rother, Jan"],["dc.contributor.author","Oelkers, Marieelen"],["dc.contributor.author","Fichtner, Dagmar"],["dc.contributor.author","Wedlich, Doris"],["dc.contributor.author","Janshoff, Andreas"],["dc.date.accessioned","2018-11-07T09:16:39Z"],["dc.date.available","2018-11-07T09:16:39Z"],["dc.date.issued","2013"],["dc.description.abstract","Structural alterations during epithelial-to-mesenchymal transition (EMT) pose a substantial challenge to the mechanical response of cells and are supposed to be key parameters for an increased malignancy during metastasis. Herein, we report that during EMT, apical tension of the epithelial cell line NMuMG is controlled by cell-cell contacts and the architecture of the underlying actin structures reflecting the mechanistic interplay between cellular structure and mechanics. Using force spectroscopy we find that tension in NMuMG cells slightly increases 24 h after EMT induction, whereas upon reaching the final mesenchymal-like state characterized by a complete loss of intercellular junctions and a concerted down-regulation of the adherens junction protein E-cadherin, the overall tension becomes similar to that of solitary adherent cells and fibroblasts. Interestingly, the contribution of the actin cytoskeleton on apical tension increases significantly upon EMT induction, most likely due to the formation of stable and highly contractile stress fibers which dominate the elastic properties of the cells after the transition. The structural alterations lead to the formation of single, highly motile cells rendering apical tension a good indicator for the cellular state during phenotype switching. In summary, our study paves the way towards a more profound understanding of cellular mechanics governing fundamental morphological programs such as the EMT."],["dc.description.sponsorship","Open-Acces-Publikationsfonds 2013"],["dc.identifier.doi","10.1371/journal.pone.0080068"],["dc.identifier.isi","000328566100009"],["dc.identifier.pmid","24339870"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9505"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27979"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Tension Monitoring during Epithelial-to-Mesenchymal Transition Links the Switch of Phenotype to Expression of Moesin and Cadherins in NMuMG Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","130084"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Open Biology"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Pietuch, Anna"],["dc.contributor.author","Janshoff, Andreas"],["dc.date.accessioned","2018-11-07T09:22:39Z"],["dc.date.available","2018-11-07T09:22:39Z"],["dc.date.issued","2013"],["dc.description.abstract","Cellular adhesion and motility are fundamental processes in biological systems such as morphogenesis and tissue homeostasis. During these processes, cells heavily rely on the ability to deform and supply plasma membrane from pre-existing membrane reservoirs, allowing the cell to cope with substantial morphological changes. While morphological changes during single cell adhesion and spreading are well characterized, the accompanying alterations in cellular mechanics are scarcely addressed. Using the atomic force microscope, we measured changes in cortical and plasma membrane mechanics during the transition from early adhesion to a fully spread cell. During the initial adhesion step, we found that tremendous changes occur in cortical and membrane tension as well as in membrane area. Monitoring the spreading progress by means of force measurements over 2.5 h reveals that cortical and membrane tension become constant at the expense of excess membrane area. This was confirmed by fluorescence microscopy, which shows a rougher plasma membrane of cells in suspension compared with spread ones, allowing the cell to draw excess membrane from reservoirs such as invaginations or protrusions while attaching to the substrate and forming a first contact zone. Concretely, we found that cell spreading is initiated by a transient drop in tension, which is compensated by a decrease in excess area. Finally, all mechanical parameters become almost constant although morphological changes continue. Our study shows how a single cell responds to alterations in membrane tension by adjusting its overall membrane area. Interference with cytoskeletal integrity, membrane tension and excess surface area by administration of corresponding small molecular inhibitors leads to perturbations of the spreading process."],["dc.identifier.doi","10.1098/rsob.130084"],["dc.identifier.isi","000325975300004"],["dc.identifier.pmid","23864554"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10727"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29396"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Royal Soc"],["dc.relation.issn","2046-2441"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Mechanics of spreading cells probed by atomic force microscopy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","11490"],["dc.bibliographiccitation.issue","48"],["dc.bibliographiccitation.journal","Soft Matter"],["dc.bibliographiccitation.lastpage","11502"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Pietuch, Anna"],["dc.contributor.author","Brueckner, Bastian Rouven"],["dc.contributor.author","Fine, Tamir"],["dc.contributor.author","Mey, Ingo"],["dc.contributor.author","Janshoff, Andreas"],["dc.date.accessioned","2018-11-07T09:29:30Z"],["dc.date.available","2018-11-07T09:29:30Z"],["dc.date.issued","2013"],["dc.description.abstract","Epithelial cells usually form a dense continuous cobblestone-like sheet that is frequently exposed to a variety of mechanical challenges encompassing osmotic stress and external forces. The response to external forces was investigated and the question of how individual polar epithelial cells organized in confluent monolayers respond to pharmaceutical stimuli targeting the key players of cellular mechanics was answered. In particular, we ask how epithelial cells respond to changes in cortical and membrane tension by surface area regulation if challenged by diverse chemical and mechanical cues. Here, a tension-based model is used that allows capturing the relevant modes of cell deformation. Together with independent measurements of membrane tension, cortical tension and excess surface area of confluent MDCK II cells it is possible to draw a mechanistic picture of how confluent cells respond to mechanical stimuli in general. Changes in tension are provoked by external stimuli directed towards the contractile actomyosin cortex (cytochalasin D, blebbistatin), and changes in the excess surface area are produced by cholesterol extraction (methyl-beta-cyclodextrin) or inhibition of dynamin (dynasore). A combination of AFM-indentation experiments with membrane-tether pulling at the same position allowed us to simultaneously monitor changes in membrane tension, cortical tension and excess surface area. Generally, we observed that removing or producing excess surface area of the plasma membrane readily adjusts membrane tension that is pivotal for the mechanical response of confluent cells. We found that isolated apical membranes from confluent MDCK II monolayers display similar mechanical properties as the apical side of living MDCK II cells in a confluent monolayer confirming that membrane mechanics in conjunction with cytoskeletal adhesion dominates the elastic response of confluent epithelial cells at large strain."],["dc.identifier.doi","10.1039/c3sm51610e"],["dc.identifier.isi","000327500200008"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10829"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31051"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Royal Soc Chemistry"],["dc.relation.issn","1744-6848"],["dc.relation.issn","1744-683X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Elastic properties of cells in the context of confluent cell monolayers: impact of tension and surface area regulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","14700"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Brueckner, Bastian Rouven"],["dc.contributor.author","Pietuch, Anna"],["dc.contributor.author","Nehls, Stefan"],["dc.contributor.author","Rother, Jan"],["dc.contributor.author","Janshoff, Andreas"],["dc.date.accessioned","2018-11-07T09:50:22Z"],["dc.date.available","2018-11-07T09:50:22Z"],["dc.date.issued","2015"],["dc.description.abstract","Plasma membrane tension is responsible for a variety of cellular functions such as motility, cell division, and endocytosis. Since membrane tension is dominated by the attachment of the actin cortex to the inner leaflet of the plasma membrane, we investigated the importance of ezrin, a major cross-linker of the membrane-cytoskeleton interface, for cellular mechanics of confluent MDCK II cells. For this purpose, we carried out ezrin depletion experiments and also enhanced the number of active ezrin molecules at the interface. Mechanical properties were assessed by force indentation experiments followed by membrane tether extraction. PIP2 micelles were injected into individual living cells to reinforce the linkage between plasma membrane and actin-cortex, while weakening of this connection was reached by ezrin siRNA and administration of the inhibitors neomycin and NSC 668394, respectively. We observed substantial stiffening of cells and an increase in membrane tension after addition of PIP2 micelles. In contrast, reduction of active ezrin led to a decrease of membrane tension accompanied by loss of excess surface area, increase in cortical tension, remodelling of actin cytoskeleton, and reduction of cell height. The data confirm the importance of the ezrin-mediated connection between plasma membrane and cortex for cellular mechanics and cell morphology."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1038/srep14700"],["dc.identifier.isi","000362173300001"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12274"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35692"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2045-2322"],["dc.rights.access","openAccess"],["dc.title","Ezrin is a Major Regulator of Membrane Tension in Epithelial Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]