Related Experiment Video

Updated: Nov 15, 2025

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection
07:38

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection

Published on: May 10, 2024

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Phosphorylation of the MNK1 substrate eIF4E is not required for response to acute pancreatitis

Amandine Alard1, Manon Strehaïano1, David Müller1

  • 1INSERM UMR-1037, Université de Toulouse, Centre de Recherches en Cancérologie de Toulouse (CRCT), Equipe Labellisée Ligue Contre le Cancer, Laboratoire d'Excellence Toulouse Cancer (TOUCAN), Toulouse, France.

Pancreatology : Official Journal of the International Association of Pancreatology (IAP) ... [Et Al.]
|March 2, 2021
PubMed
Abstract

Insights

The study investigated the role of eIF4E phosphorylation in pancreatitis. Results show that blocking this pathway does not affect pancreatitis severity, suggesting MNK1 kinase acts via other substrates in this condition.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Gastroenterology

Background:

  • Mitogen-activated protein kinase (MAPK) pathway activates MNK1 kinase, which is expressed in pancreatic acinar cells.
  • MNK1 and MAPK pathways are crucial for pancreatitis response, indicating therapeutic potential.
  • eIF4E (eukaryotic translation initiation factor 4E) is a known MNK1 substrate, suggesting its phosphorylation mediates protection in pancreatitis.

Purpose of the Study:

  • To investigate the role of eIF4E phosphorylation in acute pancreatitis.
  • To determine if MNK1 kinase's protective function in pancreatitis is mediated through eIF4E phosphorylation.

Main Methods:

  • Acute pancreatitis induced by cerulein in wild-type and Eif4e non-phosphorylatable mutant mice.
  • Western blotting used to assess MNK1-eIF4E pathway protein expression and phosphorylation.
  • Pancreatitis severity evaluated by serum amylase levels, histopathology, apoptosis, and immune infiltrate markers.

Main Results:

  • MNK1 kinase activity was significantly induced in both wild-type and transgenic mice.
  • Preventing eIF4E phosphorylation had no discernible effect on acute pancreatitis severity.
  • Serum amylase levels, acinar cell apoptosis, and immune infiltrate were comparable between genotypes.

Conclusions:

  • eIF4E phosphorylation is not essential for the response to acute pancreatitis.
  • The acinar-cell-specific MNK1 kinase likely regulates acute pancreatitis through alternative substrates.
  • This finding redirects research towards other MNK1 substrates for pancreatitis therapeutic strategies.
Keywords:
Acute pancreatitisMNK1eIF4E

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