Please use this identifier to cite or link to this item: https://doi.org/10.1021/acsbiomaterials.1c00251
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dc.titleEnhancement of Endothelialization by Topographical Features Is Mediated by PTP1B-Dependent Endothelial Adherens Junctions Remodeling
dc.contributor.authorGorji, A
dc.contributor.authorToh, PJY
dc.contributor.authorOng, HT
dc.contributor.authorToh, YC
dc.contributor.authorToyama, Y
dc.contributor.authorKanchanawong, P
dc.date.accessioned2021-07-13T08:22:37Z
dc.date.available2021-07-13T08:22:37Z
dc.date.issued2021-01-01
dc.identifier.citationGorji, A, Toh, PJY, Ong, HT, Toh, YC, Toyama, Y, Kanchanawong, P (2021-01-01). Enhancement of Endothelialization by Topographical Features Is Mediated by PTP1B-Dependent Endothelial Adherens Junctions Remodeling. ACS Biomaterials Science and Engineering 7 (6) : 2661-2675. ScholarBank@NUS Repository. https://doi.org/10.1021/acsbiomaterials.1c00251
dc.identifier.issn23739878
dc.identifier.issn23739878
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/194052
dc.description.abstractEndothelial Cells (ECs) form cohesive cellular lining of the vasculature and play essential roles in both developmental processes and pathological conditions. Collective migration and proliferation of endothelial cells (ECs) are key processes underlying endothelialization of vessels as well as vascular graft, but the complex interplay of mechanical and biochemical signals regulating these processes are still not fully elucidated. While surface topography and biochemical modifications have been used to enhance endothelialization in vitro, thus far such single-modality modifications have met with limited success. As combination therapy that utilizes multiple modalities has shown improvement in addressing various intractable and complex biomedical conditions, here, we explore a combined strategy that utilizes topographical features in conjunction with pharmacological perturbations. We characterized EC behaviors in response to micrometer-scale grating topography in concert with pharmacological perturbations of endothelial adherens junctions (EAJ) regulators. We found that the protein tyrosine phosphatase, PTP1B, serves as a potent regulator of EAJ stability, with PTP1B inhibition synergizing with grating topographies to modulate EAJ rearrangement, thereby augmenting global EC monolayer sheet orientation, proliferation, connectivity, and collective cell migration. Our data delineates the crosstalk between cell-ECM topography sensing and cell-cell junction integrity maintenance and suggests that the combined use of grating topography and PTP1B inhibitor could be a promising strategy for promoting collective EC migration and proliferation.
dc.publisherAmerican Chemical Society (ACS)
dc.sourceElements
dc.subjectPTP1B
dc.subjectVE-cadherin
dc.subjectendothelial cells
dc.subjectendothelial integrity
dc.subjectprotein tyrosine phosphatase
dc.subjecttopography sensing
dc.subjectAdherens Junctions
dc.subjectCell Line
dc.subjectCell Movement
dc.subjectEndothelial Cells
dc.subjectEndothelium, Vascular
dc.typeArticle
dc.date.updated2021-07-13T08:04:15Z
dc.contributor.departmentBIOENGINEERING
dc.contributor.departmentDEPT OF BIOLOGICAL SCIENCES
dc.contributor.departmentDEPT OF BIOMEDICAL ENGINEERING
dc.contributor.departmentMECHANOBIOLOGY INSTITUTE
dc.description.doi10.1021/acsbiomaterials.1c00251
dc.description.sourcetitleACS Biomaterials Science and Engineering
dc.description.volume7
dc.description.issue6
dc.description.page2661-2675
dc.published.statePublished
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