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dc.contributor.authorTam, Sze Noken_US
dc.date.accessioned2018-02-13T15:36:55Z
dc.date.available2018-02-13T15:36:55Z
dc.date.issued2017
dc.identifier.urihttps://hdl.handle.net/2144/27003
dc.description.abstractVarious types of mammalian cells have an exceptional ability to adapt to externally applied mechanical stresses and strains. Because of this adaptation, cells can maintain their endogenous cytoskeletal stress at a preferred (homeostatic) state. This homeostasis of mechanical stress in cells, also known as tensional homeostasis, is essential for normal physiological functions of cells and tissues and provides protection against certain diseases. Recent experimental studies revealed a novel finding that isolated endothelial cells cannot maintain tensional homeostasis, whereas multicellular clusters can. Increasing size of the multicellular clusters played a critical role in attenuating temporal fluctuations of intracellular tension as it approached homeostasis. Here, we propose to interpret these experimental results with simple mathematical models and to gain insight into factors that contribute to homeostasis. The proposed models investigate solely on how mechanical interactions between cells influence tensional homeostasis and do not consider other physical and chemical factors such as biochemical signaling and substrate rigidity. Results of our model corroborated our earlier experimental findings that tensional homeostasis is multicellular phenomenon. We were able to identify two mechanisms that influence tensional homeostasis in confluent clusters, namely statistical averaging of stress fluctuations and stress buildup in the cluster that resulted from unbalanced portion of cell-substrate tractions at the cluster boundaries. To further investigate the role of cell-cell interactions in tensional homeostasis, we conducted traction measurements in thrombin-treated endothelial cells using micropatterned traction microscopy. Our expectation was that the presence of thrombin would stimulate cellular contractility to the point of severance of cell-cell adhesions. To our surprise, the cell-cell junctions remained intact. However, the measurements revealed a threshold in the cluster size after which attenuation in cellular tension rapidly progressed. The underlying mechanism that caused the presence of a threshold is still unknown. Current efforts of our research group are dedicated to reveal and understand those mechanisms.en_US
dc.language.isoen_US
dc.subjectEngineeringen_US
dc.subjectCell-cell couplingen_US
dc.titleIdentifying factors that promote tensional homeostasis in endothelial cellsen_US
dc.typeThesis/Dissertationen_US
dc.date.updated2017-11-02T22:14:34Z
etd.degree.nameMaster of Scienceen_US
etd.degree.levelmastersen_US
etd.degree.disciplineBiomedical Engineeringen_US
etd.degree.grantorBoston Universityen_US


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