Document Detail


A single progenitor population switches behavior to maintain and repair esophageal epithelium.
MedLine Citation:
PMID:  22821983     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Diseases of the esophageal epithelium (EE), such as reflux esophagitis and cancer, are rising in incidence. Despite this, the cellular behaviors underlying EE homeostasis and repair remain controversial. Here, we show that in mice, EE is maintained by a single population of cells that divide stochastically to generate proliferating and differentiating daughters with equal probability. In response to challenge with all-trans retinoic acid (atRA), the balance of daughter cell fate is unaltered, but the rate of cell division increases. However, after wounding, cells reversibly switch to producing an excess of proliferating daughters until the wound has closed. Such fate-switching enables a single progenitor population to both maintain and repair tissue without the need for a "reserve" slow-cycling stem cell pool.
Authors:
David P Doupé; Maria P Alcolea; Amit Roshan; Gen Zhang; Allon M Klein; Benjamin D Simons; Philip H Jones
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-07-19
Journal Detail:
Title:  Science (New York, N.Y.)     Volume:  337     ISSN:  1095-9203     ISO Abbreviation:  Science     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-08-31     Completed Date:  2012-09-17     Revised Date:  2014-02-24    
Medline Journal Info:
Nlm Unique ID:  0404511     Medline TA:  Science     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1091-3     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Biological Markers / analysis
Cell Differentiation / drug effects
Cell Division / drug effects
Cell Proliferation / drug effects
Cells, Cultured
Doxycycline / pharmacology
Epithelial Cells / physiology*
Epithelium / drug effects,  metabolism,  physiology*
Esophagus / cytology*,  physiology*
Green Fluorescent Proteins / biosynthesis
Histones / biosynthesis
Mice
Mice, Inbred C57BL
Recombinant Fusion Proteins / biosynthesis
Regeneration*
Stem Cells / metabolism,  physiology*
Grant Support
ID/Acronym/Agency:
079249//Wellcome Trust; 092096//Wellcome Trust; G0601740//Medical Research Council; G0800784//Medical Research Council; MC_U105370181//Medical Research Council; U.1053.00.010(70181)//Medical Research Council; //Medical Research Council; //Wellcome Trust
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Histones; 0/Recombinant Fusion Proteins; 0/enhanced green fluorescent protein; 147336-22-9/Green Fluorescent Proteins; N12000U13O/Doxycycline
Comments/Corrections
Comment In:
Science. 2012 Aug 31;337(6098):1051-2   [PMID:  22936766 ]
Cell Stem Cell. 2012 Sep 7;11(3):284-6   [PMID:  22958926 ]
EMBO J. 2012 Sep 12;31(18):3653-4   [PMID:  22885597 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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