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Article: Protection of cerulein-induced pancreatic fibrosis by pancreas-specific expression of Smad7

TitleProtection of cerulein-induced pancreatic fibrosis by pancreas-specific expression of Smad7
Authors
KeywordsSpecies Index: Mus Musculus
Issue Date2009
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/bbadis
Citation
Biochimica et Biophysica Acta - Molecular Basis of Disease, 2009, v. 1792 n. 1, p. 56-60 How to Cite?
AbstractPancreatic fibrosis is the hallmark of chronic pancreatitis, currently an incurable disease. Pancreatitis fibrosis is caused by deposition of extracellular matrix (ECM) and the underlying pathological mechanism remains unclear. In addition to its broad biological activities, TGF-β is a potent pro-fibrotic factor and many in vitro studies using cell systems have implicated a functional role of TGF-β in the pathogenesis of pancreatic fibrosis. We analyzed the in vivo role of TGF-β pathway in pancreatic fibrosis in this study. Smad7, an intracellular inhibitory protein that antagonizes TGF-β signaling, was specifically expressed in the pancreas using a transgenic mouse model. Chronic pancreatitis was induced in the mouse with repeated administration of cerulein. Smad7 expression in the pancreas was able to significantly inhibit cerulein-induced pancreatic fibrosis. Consistently, the protein levels of collagen I and fibronectin were decreased in the Smad7 transgenic mice. In addition, α-smooth muscle actin, a marker of activated pancreas stellate cells, was reduced in the transgenic mice. Taken together, these data indicate that inhibition of TGF-β signaling by Smad7 is able to protect cerulein-induced pancreatic fibrosis in vivo. © 2008 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/92185
ISSN
2015 Impact Factor: 5.158
2015 SCImago Journal Rankings: 2.718
ISI Accession Number ID
Funding AgencyGrant Number
Chinese Academy of SciencesKSCX1-YW-02
National Natural Science Foundation of China30588002
Science and Technology Commission of Shanghai Municipality06XD14022
07DJ14005
Ministry of Science and Technology of China2006CB503900
2007013947100
Funding Information:

This work was supported by research grants from Chinese Academy of Sciences (Knowledge Innovation Program KSCX1-YW-02), National Natural Science Foundation of China (30588002), Science and Technology Commission of Shanghai Municipality (06XD14022 and 07DJ14005), and the Ministry of Science and Technology of China (2006CB503900 and 2007013947100) to YC.

References

 

DC FieldValueLanguage
dc.contributor.authorHe, Jen_HK
dc.contributor.authorSun, Xen_HK
dc.contributor.authorQian, K-Qen_HK
dc.contributor.authorLiu, Xen_HK
dc.contributor.authorWang, Zen_HK
dc.contributor.authorChen, Yen_HK
dc.date.accessioned2010-09-17T10:38:34Z-
dc.date.available2010-09-17T10:38:34Z-
dc.date.issued2009en_HK
dc.identifier.citationBiochimica et Biophysica Acta - Molecular Basis of Disease, 2009, v. 1792 n. 1, p. 56-60en_HK
dc.identifier.issn0925-4439en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92185-
dc.description.abstractPancreatic fibrosis is the hallmark of chronic pancreatitis, currently an incurable disease. Pancreatitis fibrosis is caused by deposition of extracellular matrix (ECM) and the underlying pathological mechanism remains unclear. In addition to its broad biological activities, TGF-β is a potent pro-fibrotic factor and many in vitro studies using cell systems have implicated a functional role of TGF-β in the pathogenesis of pancreatic fibrosis. We analyzed the in vivo role of TGF-β pathway in pancreatic fibrosis in this study. Smad7, an intracellular inhibitory protein that antagonizes TGF-β signaling, was specifically expressed in the pancreas using a transgenic mouse model. Chronic pancreatitis was induced in the mouse with repeated administration of cerulein. Smad7 expression in the pancreas was able to significantly inhibit cerulein-induced pancreatic fibrosis. Consistently, the protein levels of collagen I and fibronectin were decreased in the Smad7 transgenic mice. In addition, α-smooth muscle actin, a marker of activated pancreas stellate cells, was reduced in the transgenic mice. Taken together, these data indicate that inhibition of TGF-β signaling by Smad7 is able to protect cerulein-induced pancreatic fibrosis in vivo. © 2008 Elsevier B.V. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/bbadisen_HK
dc.relation.ispartofBiochimica et Biophysica Acta - Molecular Basis of Diseaseen_HK
dc.subjectSpecies Index: Mus Musculusen_HK
dc.titleProtection of cerulein-induced pancreatic fibrosis by pancreas-specific expression of Smad7en_HK
dc.typeArticleen_HK
dc.identifier.emailChen, Y:ychenc@hkucc.hku.hken_HK
dc.identifier.authorityChen, Y=rp1318en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.bbadis.2008.10.010en_HK
dc.identifier.pmid19015026-
dc.identifier.scopuseid_2-s2.0-58049221147en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-58049221147&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume1792en_HK
dc.identifier.issue1en_HK
dc.identifier.spage56en_HK
dc.identifier.epage60en_HK
dc.identifier.isiWOS:000262547900007-

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