Cell membrane disruption stimulates NO/PKG signaling and potentiates cell membrane repair in neighboring cells.

Resealing of a disrupted plasma membrane at the micron-diameter range requires Ca(2+)-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 potentia...

Full description

Bibliographic Details
Main Author: Tatsuru Togo
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3413670?pdf=render
id doaj-66c6a00aa91f4aa6a688f3bf18d6472e
record_format Article
spelling doaj-66c6a00aa91f4aa6a688f3bf18d6472e2020-11-25T01:46:18ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0178e4288510.1371/journal.pone.0042885Cell membrane disruption stimulates NO/PKG signaling and potentiates cell membrane repair in neighboring cells.Tatsuru TogoResealing of a disrupted plasma membrane at the micron-diameter range requires Ca(2+)-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.http://europepmc.org/articles/PMC3413670?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Tatsuru Togo
spellingShingle Tatsuru Togo
Cell membrane disruption stimulates NO/PKG signaling and potentiates cell membrane repair in neighboring cells.
PLoS ONE
author_facet Tatsuru Togo
author_sort Tatsuru Togo
title Cell membrane disruption stimulates NO/PKG signaling and potentiates cell membrane repair in neighboring cells.
title_short Cell membrane disruption stimulates NO/PKG signaling and potentiates cell membrane repair in neighboring cells.
title_full Cell membrane disruption stimulates NO/PKG signaling and potentiates cell membrane repair in neighboring cells.
title_fullStr Cell membrane disruption stimulates NO/PKG signaling and potentiates cell membrane repair in neighboring cells.
title_full_unstemmed Cell membrane disruption stimulates NO/PKG signaling and potentiates cell membrane repair in neighboring cells.
title_sort cell membrane disruption stimulates no/pkg signaling and potentiates cell membrane repair in neighboring cells.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2012-01-01
description Resealing of a disrupted plasma membrane at the micron-diameter range requires Ca(2+)-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.
url http://europepmc.org/articles/PMC3413670?pdf=render
work_keys_str_mv AT tatsurutogo cellmembranedisruptionstimulatesnopkgsignalingandpotentiatescellmembranerepairinneighboringcells
_version_ 1725020393846079488