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dc.contributor.authorTogo, Tatsuru
dc.contributor.editorMcNeil, Paul L.
dc.date.accessioned2012-10-26T16:40:54Z
dc.date.available2012-10-26T16:40:54Z
dc.date.issued2012-08-7en_US
dc.identifier.citationPLoS One. 2012 Aug 7; 7(8):e42885en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid22880128en_US
dc.identifier.doi10.1371/journal.pone.0042885en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/725
dc.description.abstractResealing of a disrupted plasma membrane at the micron-diameter range requires Ca2+-regulated exocytosis. Repeated membrane disruptions reseal more quickly than the initial wound, and this potentiation of membrane resealing persists for at least 24 hours after the initial wound. Long-term potentiation of membrane resealing requires CREB-dependent gene expression, which is activated by the PKC- and p38 MAPK-dependent pathway in a wounded cell. The present study demonstrates that membrane resealing is potentiated in both wounded and neighboring cells in MDCK cells. Wounding of cells expressing CREB133, a mutant variant of CREB, does not show the potentiated response of cell membrane resealing in either wounded or neighboring cells. Furthermore, wounding of cells induces CREB phosphorylation, not only in wounded cells, but also in neighboring cells. Inhibition of the nitric oxide/PKG signaling pathway suppresses CREB phosphorylation in neighboring cells, but not in wounded cells. The potentiation of membrane resealing in neighboring cells is suppressed if the nitric oxide/PKG pathway is inhibited during the initial wound. Together, these results suggest that the nitric oxide/PKG pathway stimulates CREB phosphorylation in neighboring cells so that subsequent cell membrane disruptions of the neighboring cells reseal more quickly.
dc.subjectResearch Articleen_US
dc.subjectBiologyen_US
dc.subjectBiochemistryen_US
dc.subjectCytochemistryen_US
dc.subjectCell Membraneen_US
dc.subjectMembrane Metabolismen_US
dc.subjectMolecular Cell Biologyen_US
dc.subjectCellular Typesen_US
dc.subjectEpithelial Cellsen_US
dc.subjectSignal Transductionen_US
dc.subjectSignaling Cascadesen_US
dc.subjectProtein Kinase Signaling Cascadeen_US
dc.subjectSignaling in Cellular Processesen_US
dc.subjectCreb Signalingen_US
dc.subjectcGMP signalingen_US
dc.subjectCellular Stress Responsesen_US
dc.titleCell Membrane Disruption Stimulates NO/PKG Signaling and Potentiates Cell Membrane Repair in Neighboring Cellsen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3413670en_US
dc.contributor.corporatenameDepartment of Cellular Biology and Anatomy
refterms.dateFOA2019-04-10T00:40:38Z
html.description.abstractResealing of a disrupted plasma membrane at the micron-diameter range requires Ca2+-regulated exocytosis. Repeated membrane disruptions reseal more quickly than the initial wound, and this potentiation of membrane resealing persists for at least 24 hours after the initial wound. Long-term potentiation of membrane resealing requires CREB-dependent gene expression, which is activated by the PKC- and p38 MAPK-dependent pathway in a wounded cell. The present study demonstrates that membrane resealing is potentiated in both wounded and neighboring cells in MDCK cells. Wounding of cells expressing CREB133, a mutant variant of CREB, does not show the potentiated response of cell membrane resealing in either wounded or neighboring cells. Furthermore, wounding of cells induces CREB phosphorylation, not only in wounded cells, but also in neighboring cells. Inhibition of the nitric oxide/PKG signaling pathway suppresses CREB phosphorylation in neighboring cells, but not in wounded cells. The potentiation of membrane resealing in neighboring cells is suppressed if the nitric oxide/PKG pathway is inhibited during the initial wound. Together, these results suggest that the nitric oxide/PKG pathway stimulates CREB phosphorylation in neighboring cells so that subsequent cell membrane disruptions of the neighboring cells reseal more quickly.


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