Skip to main navigation Skip to search Skip to main content

Identification of candidate genes involved in endogenous protection mechanisms against acute pancreatitis in mice

  • Shinji Nakada
  • , Koichi Tsuneyama
  • , Ichiro Kato
  • , Yoshiaki Tabuchi
  • , Ichiro Takasaki
  • , Yukihiro Furusawa
  • , Hiroshi Kawaguchi
  • , Makoto Fujimoto
  • , Hirozo Goto
  • , Hiroaki Hikiami
  • , Takashi Kondo
  • , Yasuo Takano
  • , Yutaka Shimada

Research output: Contribution to journalArticlepeer-review

Abstract

We surveyed changes of the gene expression profile in caerulein-exposed pancreas using Affymetrix GeneChip system (39,000 genes). Up-regulation of genes coding for claudin 4, claudin 7, F11 receptor, cadherin 1, integrin beta 4, syndecan 1, heat shock proteins b1/90aa1, Serpinb6a, Serpinb6b, Serpinb9, Bax, Bak1, calpain 2, calpain 5, microtubule-associated protein 1 light chain 3 alpha, S100 calcium-binding proteins A4/A10 were found in mouse pancreas exposed to caerulein for 12 h. In contrast, the anti-apoptotic gene Bcl2 was down-regulated. The functions of these genes concern tight junction formation, cell-cell/cell-matrix adhesions, stress response, protease inhibition, apoptosis, autophagy, and regulation of cytoskeletal dynamics. Caerulein-exposed pancreatic acinar cells were immunohistochemically stained for claudin 4, cadherin 1, integrin beta 4, heat shock protein b1, and Serpinb6a. In conclusion, we have newly identified a set of genes that are likely to be involved in endogenous self-protection mechanisms against acute pancreatitis.

Original languageEnglish
Pages (from-to)1342-1347
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume391
Issue number3
DOIs
Publication statusPublished - 2010 Jan 15

Keywords

  • Caerulein
  • Claudin
  • GeneChip
  • Heat shock protein
  • Pancreatitis
  • Protease inhibitor

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Fingerprint

Dive into the research topics of 'Identification of candidate genes involved in endogenous protection mechanisms against acute pancreatitis in mice'. Together they form a unique fingerprint.

Cite this