AustralieFrV1, Ncbi, Checkpoint, bibRecord, 000356

Hepatocyte nuclear factor 4α in the intestinal epithelial cells protects against inflammatory bowel disease

Identifieur interne : 000356 ( Ncbi/Checkpoint ); précédent : 000355; suivant : 000357

Hepatocyte nuclear factor 4α in the intestinal epithelial cells protects against inflammatory bowel disease

Auteurs : Sung-Hoon Ahn [États-Unis] ; Yatrik M. Shah [États-Unis] ; Junko Inoue [États-Unis] ; Keiichiro Morimura [États-Unis, Japon] ; Insook Kim [États-Unis] ; Sunhee Yim [États-Unis] ; Gilles Lambert [Australie] ; Reiko Kurotani [États-Unis, Japon] ; Kunio Nagashima [États-Unis] ; Frank J. Gonzalez [États-Unis] ; Yusuke Inoue [États-Unis]

Source :

Inflammatory bowel diseases [ 1078-0998 ] ; 2008.

RBID : PMC:2435391

Abstract

Background

Hepatocyte nuclear factor 4α (HNF4α; NR2A1) is an orphan member of the nuclear receptor superfamily expressed in liver and intestine. While HNF4α expression is critical for liver function, its role in the gut and in the pathogenesis of inflammatory bowel disease (IBD) is unknown.

Methods

Human intestinal biopsies from control and IBD patients were examined for expression of mRNAs encoding HNF4α and other nuclear receptors. An intestine-specific HNF4α null mouse line (Hnf4α^ΔIEpC) was generated using an Hnf4α-floxed allele and villin-Cre transgene. These mice and their control floxed counterparts (Hnf4α^F/F), were subjected to a dextran sulfate sodium (DSS)-induced IBD colitis protocol and their clinical symptoms and gene expression patterns determined.

Results

In human intestinal biopsies, HNF4α was significantly decreased in intestinal tissues from Crohn’s disease and ulcerative colitis patients. HNF4α expression was also suppressed in the intestine of DSS-treated mice. In Hnf4α^ΔIEpC mice, disruption of HNF4α expression was observed in the epithelial cells throughout intestine. In the DSS-induced colitis model, Hnf4α^ΔIEpC mice showed markedly more severe changes in clinical symptoms and pathologies associated with IBD including loss of body weight, colon length, and histological morphology, as compared with Hnf4α^F/F mice. Furthermore the Hnf4α^ΔIEpC mice demonstrate a significant alteration of mucin associated genes and increase intestinal permeability, which may play an important role in the increased susceptibility to acute colitis following an inflammatory insult.

Conclusions

While HNF4α does not have a major role in normal function of the intestine, it protects the gut against DSS-induced colitis.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2435391

DOI: 10.1002/ibd.20413
PubMed: 18338782
PubMed Central: 2435391

Affiliations:

Australie, Japon, États-Unis
Maryland

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PMC:2435391

Le document en format XML

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<author><name sortKey="Gonzalez, Frank J" sort="Gonzalez, Frank J" uniqKey="Gonzalez F" first="Frank J." last="Gonzalez">Frank J. Gonzalez</name>
<affiliation wicri:level="2"><nlm:aff id="A1"> Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Maryland</region>
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<author><name sortKey="Inoue, Yusuke" sort="Inoue, Yusuke" uniqKey="Inoue Y" first="Yusuke" last="Inoue">Yusuke Inoue</name>
<affiliation wicri:level="2"><nlm:aff id="A1"> Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Maryland</region>
</placeName>
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</affiliation>
<affiliation><nlm:aff id="A6"> Department of Chemistry and Chemical Biology, Graduate School of Engineering, Gunma University, Kiryu, Gunma 376-8515 Japan</nlm:aff>
<wicri:noCountry code="subfield">Gunma 376-8515 Japan</wicri:noCountry>
</affiliation>
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<series><title level="j">Inflammatory bowel diseases</title>
<idno type="ISSN">1078-0998</idno>
<idno type="eISSN">1536-4844</idno>
<imprint><date when="2008">2008</date>
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title>
<p id="P1">Hepatocyte nuclear factor 4α (HNF4α; NR2A1) is an orphan member of the nuclear receptor superfamily expressed in liver and intestine. While HNF4α expression is critical for liver function, its role in the gut and in the pathogenesis of inflammatory bowel disease (IBD) is unknown.</p>
</sec>
<sec sec-type="methods" id="S2"><title>Methods</title>
<p id="P2">Human intestinal biopsies from control and IBD patients were examined for expression of mRNAs encoding HNF4α and other nuclear receptors. An intestine-specific HNF4α null mouse line (<italic>Hnf4α</italic>
<sup>ΔIEpC</sup>
) was generated using an <italic>Hnf4α</italic>
-floxed allele and villin-Cre transgene. These mice and their control floxed counterparts (<italic>Hnf4α</italic>
<sup>F/F</sup>
), were subjected to a dextran sulfate sodium (DSS)-induced IBD colitis protocol and their clinical symptoms and gene expression patterns determined.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">In human intestinal biopsies, HNF4α was significantly decreased in intestinal tissues from Crohn’s disease and ulcerative colitis patients. HNF4α expression was also suppressed in the intestine of DSS-treated mice. In <italic>Hnf4α</italic>
<sup>ΔIEpC</sup>
 mice, disruption of HNF4α expression was observed in the epithelial cells throughout intestine. In the DSS-induced colitis model, <italic>Hnf4α</italic>
<sup>ΔIEpC</sup>
 mice showed markedly more severe changes in clinical symptoms and pathologies associated with IBD including loss of body weight, colon length, and histological morphology, as compared with <italic>Hnf4α</italic>
<sup>F/F</sup>
 mice. Furthermore the <italic>Hnf4α</italic>
<sup>ΔIEpC</sup>
 mice demonstrate a significant alteration of mucin associated genes and increase intestinal permeability, which may play an important role in the increased susceptibility to acute colitis following an inflammatory insult.</p>
</sec>
<sec id="S4"><title>Conclusions</title>
<p id="P4">While HNF4α does not have a major role in normal function of the intestine, it protects the gut against DSS-induced colitis.</p>
</sec>
</div>
</front>
</TEI>
<affiliations><list><country><li>Australie</li>
<li>Japon</li>
<li>États-Unis</li>
</country>
<region><li>Maryland</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Maryland"><name sortKey="Ahn, Sung Hoon" sort="Ahn, Sung Hoon" uniqKey="Ahn S" first="Sung-Hoon" last="Ahn">Sung-Hoon Ahn</name>
</region>
<name sortKey="Gonzalez, Frank J" sort="Gonzalez, Frank J" uniqKey="Gonzalez F" first="Frank J." last="Gonzalez">Frank J. Gonzalez</name>
<name sortKey="Inoue, Junko" sort="Inoue, Junko" uniqKey="Inoue J" first="Junko" last="Inoue">Junko Inoue</name>
<name sortKey="Inoue, Yusuke" sort="Inoue, Yusuke" uniqKey="Inoue Y" first="Yusuke" last="Inoue">Yusuke Inoue</name>
<name sortKey="Kim, Insook" sort="Kim, Insook" uniqKey="Kim I" first="Insook" last="Kim">Insook Kim</name>
<name sortKey="Kurotani, Reiko" sort="Kurotani, Reiko" uniqKey="Kurotani R" first="Reiko" last="Kurotani">Reiko Kurotani</name>
<name sortKey="Morimura, Keiichiro" sort="Morimura, Keiichiro" uniqKey="Morimura K" first="Keiichiro" last="Morimura">Keiichiro Morimura</name>
<name sortKey="Nagashima, Kunio" sort="Nagashima, Kunio" uniqKey="Nagashima K" first="Kunio" last="Nagashima">Kunio Nagashima</name>
<name sortKey="Shah, Yatrik M" sort="Shah, Yatrik M" uniqKey="Shah Y" first="Yatrik M." last="Shah">Yatrik M. Shah</name>
<name sortKey="Yim, Sunhee" sort="Yim, Sunhee" uniqKey="Yim S" first="Sunhee" last="Yim">Sunhee Yim</name>
</country>
<country name="Japon"><noRegion><name sortKey="Morimura, Keiichiro" sort="Morimura, Keiichiro" uniqKey="Morimura K" first="Keiichiro" last="Morimura">Keiichiro Morimura</name>
</noRegion>
<name sortKey="Kurotani, Reiko" sort="Kurotani, Reiko" uniqKey="Kurotani R" first="Reiko" last="Kurotani">Reiko Kurotani</name>
</country>
<country name="Australie"><noRegion><name sortKey="Lambert, Gilles" sort="Lambert, Gilles" uniqKey="Lambert G" first="Gilles" last="Lambert">Gilles Lambert</name>
</noRegion>
</country>
</tree>
</affiliations>
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   |area=    AustralieFrV1
   |flux=    Ncbi
   |étape=   Checkpoint
   |type=    RBID
   |clé=     PMC:2435391
   |texte=   Hepatocyte nuclear factor 4α in the intestinal epithelial cells protects against inflammatory bowel disease
}}

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HfdIndexSelect -h $EXPLOR_AREA/Data/Ncbi/Checkpoint/RBID.i   -Sk "pubmed:18338782" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Ncbi/Checkpoint/biblio.hfd   \
       | NlmPubMed2Wicri -a AustralieFrV1

This area was generated with Dilib version V0.6.33.
Data generation: Tue Dec 5 10:43:12 2017. Site generation: Tue Mar 5 14:07:20 2024

	Serveur d'exploration sur les relations entre la France et l'Australie
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur les relations entre la France et l'Australie

Hepatocyte nuclear factor 4α in the intestinal epithelial cells protects against inflammatory bowel disease

Hepatocyte nuclear factor 4α in the intestinal epithelial cells protects against inflammatory bowel disease

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