Increased Expression of Hypoxia-Inducible Factor-1α, p48, and the Notch Signaling Cascade during Acute Pancreatitis in Mice

Guillermo Gomez, Ella W. Englander, Guiyun Wang, George H. Greeley

Research output: Contribution to journalArticle

27 Scopus citations

Abstract

Acute pancreatitis (AP) is a complex disease that may be linked to acinar cell apoptosis and inadequate acinar cell replacement. Differentiation of acinar cells is regulated by p48, a DNA binding subunit of the transcription factor PTF1, and the Notch signaling pathway. Acinar cell apoptosis is triggered by oxygen deprivation, ie, hypoxia, by activation of hypoxia inducible factor-1α (HIF-1α). The aim of this study was to characterize by Northern blot analyses expression of HIF-1α, HIF-1α-inducible genes (GLUT-1, VEGF, p53), p48, and genes involved in the Notch signaling pathway (Notch-1, D111, RBP-Jk, HES-1) during cerulein-induced AP in mice. Maximal expression of HIF-1α, HIF-1α-inducible genes, p48, and Notch signaling genes occurred 8-12 hours after induction of AP. Maximal expression of p53 occurred 12-48 hours after induction of AP. These findings demonstrate that multiple pancreatic genes are activated acutely during AP that support pancreatic cell replenishment, regulation of expression of acinar cell-specific genes, and apoptosis.

Original languageEnglish (US)
Pages (from-to)58-64
Number of pages7
JournalPancreas
Volume28
Issue number1
DOIs
StatePublished - Jan 1 2004

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Hepatology
  • Endocrinology

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