AustralieFrV1, Pmc, Corpus, bibRecord, 001E49

The CSF-1 receptor fashions the intestinal stem cell niche✩

Identifieur interne : 001E49 ( Pmc/Corpus ); précédent : 001E48; suivant : 001E50

The CSF-1 receptor fashions the intestinal stem cell niche✩

Auteurs : Dilara Akcora ; Duy Huynh ; Sally Lightowler ; Markus Germann ; Sylvie Robine ; Jan R. De May ; Jeffrey W. Pollard ; E. Richard Stanley ; Jordane Malaterre ; Robert G. Ramsay

Source :

Stem cell research [ 1873-5061 ] ; 2012.

RBID : PMC:4096353

Abstract

Gastrointestinal (GI) homeostasis requires the action of multiple pathways. There is some controversy regarding whether small intestine (SI) Paneth cells (PCs) play a central role in orchestrating crypt architecture and their relationship with Lgr5+ve stem cells. Nevertheless, we previously showed that germline CSF-1 receptor (Csf1r) knock out (KO) or Csf1 mutation is associated with an absence of mature PC, reduced crypt proliferation and lowered stem cell gene, Lgr5 expression. Here we show the additional loss of CD24, Bmi1 and Olfm4 expression in the KO crypts and a high resolution 3D localization of CSF-1R mainly to PC. The induction of GI-specific Csf1r deletion in young adult mice also led to PC loss over a period of weeks, in accord with the anticipated long life span of PC, changed distribution of proliferating cells and this was with a commensurate loss of Lgr5 and other stem cell marker gene expression. By culturing SI organoids, we further show that the Csf1r^−/− defect in PC production is intrinsic to epithelial cells as well as definitively affecting stem cell activity. These results show that CSF-1R directly supports PC maturation and that in turn PCs fashion the intestinal stem cell niche.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4096353

DOI: 10.1016/j.scr.2012.12.001
PubMed: 23314290
PubMed Central: 4096353

Links to Exploration step

PMC:4096353

Le document en format XML

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<author><name sortKey="Robine, Sylvie" sort="Robine, Sylvie" uniqKey="Robine S" first="Sylvie" last="Robine">Sylvie Robine</name>
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<affiliation><nlm:aff id="A4">Université de Strasbourg, F-67081, France</nlm:aff>
</affiliation>
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<series><title level="j">Stem cell research</title>
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<front><div type="abstract" xml:lang="en"><p id="P1">Gastrointestinal (GI) homeostasis requires the action of multiple pathways. There is some controversy regarding whether small intestine (SI) Paneth cells (PCs) play a central role in orchestrating crypt architecture and their relationship with Lgr5+ve stem cells. Nevertheless, we previously showed that germline CSF-1 receptor (<italic>Csf1r</italic>
) knock out (KO) or <italic>Csf1</italic>
 mutation is associated with an absence of mature PC, reduced crypt proliferation and lowered stem cell gene, <italic>Lgr5</italic>
 expression. Here we show the additional loss of CD24, <italic>Bmi1</italic>
 and <italic>Olfm4</italic>
 expression in the KO crypts and a high resolution 3D localization of CSF-1R mainly to PC. The induction of GI-specific <italic>Csf1r</italic>
 deletion in young adult mice also led to PC loss over a period of weeks, in accord with the anticipated long life span of PC, changed distribution of proliferating cells and this was with a commensurate loss of <italic>Lgr5</italic>
 and other stem cell marker gene expression. By culturing SI organoids, we further show that the <italic>Csf1r</italic>
<sup>−/−</sup>
 defect in PC production is intrinsic to epithelial cells as well as definitively affecting stem cell activity. These results show that CSF-1R directly supports PC maturation and that in turn PCs fashion the intestinal stem cell niche.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
  <pmc-dir>properties manuscript</pmc-dir>
  <front><journal-meta><journal-id journal-id-type="nlm-journal-id">101316957</journal-id>
<journal-id journal-id-type="pubmed-jr-id">35616</journal-id>
<journal-id journal-id-type="nlm-ta">Stem Cell Res</journal-id>
<journal-id journal-id-type="iso-abbrev">Stem Cell Res</journal-id>
<journal-title-group><journal-title>Stem cell research</journal-title>
</journal-title-group>
<issn pub-type="ppub">1873-5061</issn>
<issn pub-type="epub">1876-7753</issn>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">23314290</article-id>
<article-id pub-id-type="pmc">4096353</article-id>
<article-id pub-id-type="doi">10.1016/j.scr.2012.12.001</article-id>
<article-id pub-id-type="manuscript">NIHMS580161</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>The CSF-1 receptor fashions the intestinal stem cell niche<sup><xref ref-type="fn" rid="FN1">✩</xref>
</sup>
</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Akcora</surname>
<given-names>Dilara</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Huynh</surname>
<given-names>Duy</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Lightowler</surname>
<given-names>Sally</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Germann</surname>
<given-names>Markus</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Robine</surname>
<given-names>Sylvie</given-names>
</name>
<xref ref-type="aff" rid="A2">b</xref>
</contrib>
<contrib contrib-type="author"><name><surname>de May</surname>
<given-names>Jan R.</given-names>
</name>
<xref ref-type="aff" rid="A3">c</xref>
<xref ref-type="aff" rid="A4">d</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Pollard</surname>
<given-names>Jeffrey W.</given-names>
</name>
<xref ref-type="aff" rid="A5">e</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Stanley</surname>
<given-names>E. Richard</given-names>
</name>
<xref ref-type="aff" rid="A5">e</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Malaterre</surname>
<given-names>Jordane</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ramsay</surname>
<given-names>Robert G.</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>a</label>
Peter MacCallum Cancer Centre and the Sir Peter MacCallum Oncology Department and the Pathology Department, University of Melbourne, Australia</aff>
<aff id="A2"><label>b</label>
Centre National de la Recherche Scientifique, Institut Curie, 75248 Paris, Cedex 05, France</aff>
<aff id="A3"><label>c</label>
CNRS, UMR 7213, Laboratoire de Biophotonique et Pharmacologie, F-67401 Illkirch, France</aff>
<aff id="A4"><label>d</label>
Université de Strasbourg, F-67081, France</aff>
<aff id="A5"><label>e</label>
Albert Einstein College of Medicine, Bronx, NY 10461, USA</aff>
<author-notes><corresp id="cor1"><label>*</label>
Corresponding author at: Differentiation and Transcription laboratory, Peter MacCallum Cancer Centre, East Melbourne, 3002 Victoria, Australia. Fax: +61 3 965 1411. <email>rob.ramsay@petermac.org</email>
 (R.G. Ramsay)</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>12</day>
<month>5</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="epub"><day>09</day>
<month>12</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="ppub"><month>3</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>14</day>
<month>7</month>
<year>2014</year>
</pub-date>
<volume>10</volume>
<issue>2</issue>
<fpage>203</fpage>
<lpage>212</lpage>
<pmc-comment>elocation-id from pubmed: 10.1016/j.scr.2012.12.001</pmc-comment>
      <permissions><copyright-statement>© 2012 Elsevier B.V. All rights reserved.</copyright-statement>
<copyright-year>2012</copyright-year>
</permissions>
<abstract><p id="P1">Gastrointestinal (GI) homeostasis requires the action of multiple pathways. There is some controversy regarding whether small intestine (SI) Paneth cells (PCs) play a central role in orchestrating crypt architecture and their relationship with Lgr5+ve stem cells. Nevertheless, we previously showed that germline CSF-1 receptor (<italic>Csf1r</italic>
) knock out (KO) or <italic>Csf1</italic>
 mutation is associated with an absence of mature PC, reduced crypt proliferation and lowered stem cell gene, <italic>Lgr5</italic>
 expression. Here we show the additional loss of CD24, <italic>Bmi1</italic>
 and <italic>Olfm4</italic>
 expression in the KO crypts and a high resolution 3D localization of CSF-1R mainly to PC. The induction of GI-specific <italic>Csf1r</italic>
 deletion in young adult mice also led to PC loss over a period of weeks, in accord with the anticipated long life span of PC, changed distribution of proliferating cells and this was with a commensurate loss of <italic>Lgr5</italic>
 and other stem cell marker gene expression. By culturing SI organoids, we further show that the <italic>Csf1r</italic>
<sup>−/−</sup>
 defect in PC production is intrinsic to epithelial cells as well as definitively affecting stem cell activity. These results show that CSF-1R directly supports PC maturation and that in turn PCs fashion the intestinal stem cell niche.</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>

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The CSF-1 receptor fashions the intestinal stem cell niche✩

The CSF-1 receptor fashions the intestinal stem cell niche✩

Source :

Abstract

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki