Publication:
Loss of periostin results in impaired regeneration and pancreatic atrophy after cerulein-induced pancreatitis

dc.contributor.coauthorHausmann, Simone
dc.contributor.coauthorRegel, Ivonne
dc.contributor.coauthorSteiger, Katja
dc.contributor.coauthorWagner, Nadine
dc.contributor.coauthorThorwirth, Manja
dc.contributor.coauthorSchlitter, Anna M.
dc.contributor.coauthorEsposito, Irene
dc.contributor.coauthorMichalski, Christoph W.
dc.contributor.coauthorFriess, Helmut
dc.contributor.coauthorKleeff, Joerg
dc.contributor.departmentN/A
dc.contributor.kuauthorErkan, Murat Mert
dc.contributor.kuprofileFaculty Member
dc.contributor.schoolcollegeinstituteSchool of Medicine
dc.contributor.yokid214689
dc.date.accessioned2024-11-09T23:28:43Z
dc.date.issued2016
dc.description.abstractThe extracellular matrix molecule periostin (POSTN, encoded by POSTN), which is secreted by activated pancreatic stellate cells, has important functions in chronic pancreatitis and pancreatic cancer. However, the role of POSTN in acute pancreatitis and subsequent regeneration processes has not been addressed so far. We analyzed the function of POSTN in pancreatic exocrine regeneration after the induction of a severe acute pancreatitis. Postn-deficient mice and wild-type control animals received repetitive cerulein injections, and a detailed histologic analysis of pancreatic tissues was performed. Although there was no difference in pancreatitis severity in the acute inflammatory phase, the recovery of the exocrine pancreas was massively impaired in Postn-deficient mice. Loss of Postn expression was accompanied by strong pancreatic atrophy and acinar-to-adipocyte differentiation, which was also reflected in gene expression patterns. Our data suggest that POSTN is a crucial factor for proper exocrine lineage-specific regeneration after severe acute pancreatitis.
dc.description.indexedbyWoS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.issue1
dc.description.openaccessYES
dc.description.publisherscopeInternational
dc.description.sponsorshipBundesministerium fur Bildung und Forschung (Federal Ministry of Education and Research) [NGFN-Plus PKB-01GS08115-7]
dc.description.sponsorshipEuropean Community's Seventh Framework Programme [EPC-TM-Net 256974] Supported in part by Bundesministerium fur Bildung und Forschung (The Federal Ministry of Education and Research) grant NGFN-Plus PKB-01GS08115-7 and European Community's Seventh Framework Programme grant EPC-TM-Net 256974.
dc.description.volume186
dc.identifier.doi10.1016/j.ajpath.2015.09.022
dc.identifier.eissn1525-2191
dc.identifier.issn0002-9440
dc.identifier.quartileQ1
dc.identifier.scopus2-s2.0-84955505627
dc.identifier.urihttp://dx.doi.org/10.1016/j.ajpath.2015.09.022
dc.identifier.urihttps://hdl.handle.net/20.500.14288/11941
dc.identifier.wos367705300004
dc.keywordsInflammation
dc.keywordsExpression
dc.keywordsProtein
dc.keywordsResection
dc.keywordsFibrosis
dc.keywordsStroma
dc.keywordsCells
dc.keywordsModel
dc.languageEnglish
dc.publisherElsevier
dc.sourceAmerican Journal of Pathology
dc.subjectPathology
dc.titleLoss of periostin results in impaired regeneration and pancreatic atrophy after cerulein-induced pancreatitis
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.authorid0000-0002-2753-0234
local.contributor.kuauthorErkan, Murat Mert

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