Hdl Handle:
http://hdl.handle.net/10675.2/56
Title:
Disruption-induced mucus secretion: repair and protection.
Authors:
Miyake, Katsuya; Tanaka, Tomoaki; McNeil, Paul L.
Abstract:
When a cell suffers a plasma membrane disruption, extracellular Ca(2+) rapidly diffuses into its cytosol, triggering there local homotypic and exocytotic membrane fusion events. One role of this emergency exocytotic response is to promote cell survival: the internal membrane thus added to the plasma membrane acts as a reparative "patch." Another, unexplored consequence of disruption-induced exocytosis is secretion. Many of the cells lining the gastrointestinal tract secrete mucus via a compound exocytotic mechanism, and these and other epithelial cell types lining the digestive tract are normally subject to plasma membrane disruption injury in vivo. Here we show that plasma membrane disruption triggers a potent mucus secretory response from stomach mucous cells wounded in vitro by shear stress or by laser irradiation. This disruption-induced secretory response is Ca(2+) dependent, and coupled to cell resealing: disruption in the absence of Ca(2+) does not trigger mucus release, but results instead in cell death due to failure to reseal. Ca(2+)-dependent, disruption-induced mucus secretion and resealing were also demonstrable in segments of intact rat large intestine. We propose that, in addition to promoting cell survival of membrane disruptions, disruption-induced exocytosis serves also the important protective function of liberating lubricating mucus at sites of mechanical wear and tear. This mode of mechanotransduction can, we propose, explain how lubrication in the gastrointestinal tract is rapidly and precisely adjusted to widely fluctuating, diet-dependent levels of mechanical stress.
Citation:
PLoS Biol. 2006 Sep 22; 4(9):e276
Issue Date:
28-Aug-2006
URI:
http://hdl.handle.net/10675.2/56
DOI:
10.1371/journal.pbio.0040276
PubMed ID:
16933971
PubMed Central ID:
PMC1544361
Type:
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
ISSN:
1545-7885
Appears in Collections:
Institute of Molecular Medicine and Genetics: Faculty Research and Publications

Full metadata record

DC FieldValue Language
dc.contributor.authorMiyake, Katsuyaen_US
dc.contributor.authorTanaka, Tomoakien_US
dc.contributor.authorMcNeil, Paul L.en_US
dc.date.accessioned2010-09-24T21:26:49Z-
dc.date.available2010-09-24T21:26:49Z-
dc.date.issued2006-08-28en_US
dc.identifier.citationPLoS Biol. 2006 Sep 22; 4(9):e276en_US
dc.identifier.issn1545-7885en_US
dc.identifier.pmid16933971en_US
dc.identifier.doi10.1371/journal.pbio.0040276en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/56-
dc.description.abstractWhen a cell suffers a plasma membrane disruption, extracellular Ca(2+) rapidly diffuses into its cytosol, triggering there local homotypic and exocytotic membrane fusion events. One role of this emergency exocytotic response is to promote cell survival: the internal membrane thus added to the plasma membrane acts as a reparative "patch." Another, unexplored consequence of disruption-induced exocytosis is secretion. Many of the cells lining the gastrointestinal tract secrete mucus via a compound exocytotic mechanism, and these and other epithelial cell types lining the digestive tract are normally subject to plasma membrane disruption injury in vivo. Here we show that plasma membrane disruption triggers a potent mucus secretory response from stomach mucous cells wounded in vitro by shear stress or by laser irradiation. This disruption-induced secretory response is Ca(2+) dependent, and coupled to cell resealing: disruption in the absence of Ca(2+) does not trigger mucus release, but results instead in cell death due to failure to reseal. Ca(2+)-dependent, disruption-induced mucus secretion and resealing were also demonstrable in segments of intact rat large intestine. We propose that, in addition to promoting cell survival of membrane disruptions, disruption-induced exocytosis serves also the important protective function of liberating lubricating mucus at sites of mechanical wear and tear. This mode of mechanotransduction can, we propose, explain how lubrication in the gastrointestinal tract is rapidly and precisely adjusted to widely fluctuating, diet-dependent levels of mechanical stress.en_US
dc.rightsThe PMC Open Access Subset is a relatively small part of the total collection of articles in PMC. Articles in the PMC Open Access Subset are still protected by copyright, but are made available under a Creative Commons or similar license that generally allows more liberal redistribution and reuse than a traditional copyrighted work. Please refer to the license statement in each article for specific terms of use. The license terms are not identical for all articles in this subset.en_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium / metabolismen_US
dc.subject.meshCell Deathen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Membrane / metabolismen_US
dc.subject.meshGastric Mucosa / cytology / secretionen_US
dc.subject.meshHumansen_US
dc.subject.meshMucus / secretionen_US
dc.subject.meshRatsen_US
dc.titleDisruption-induced mucus secretion: repair and protection.en_US
dc.typeJournal Articleen_US
dc.typeResearch Support, U.S. Gov't, Non-P.H.S.en_US
dc.identifier.pmcidPMC1544361en_US
dc.contributor.corporatenameInstitute of Molecular Medicine and Geneticsen_US
dc.contributor.corporatenameDepartment of Cellular Biology and Anatomyen_US

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