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Matrix metalloproteinase secretion by gastric epithelial cells is regulated by E prostaglandins and MAPKs

Michael H Pillinger1, Nada Marjanovic, Seok-Yong Kim

  • 1Department of Medicine, New York University School of Medicine, New York, New York 10016, USA. michael.pillinger@med.nyu.edu

The Journal of Biological Chemistry
|January 11, 2005
PubMed

Insights

Matrix metalloproteinases (MMPs) contribute to gastric injury. Tumor necrosis factor-alpha and interleukin-1beta stimulate MMP-1 and MMP-13 secretion through different pathways, suggesting mechanisms for Helicobacter pylori infection and NSAID-induced gastric damage.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Cell Signaling

Background:

  • Matrix metalloproteinases (MMPs) are implicated in inflammatory tissue injury.
  • Gastric epithelial cells secrete MMPs, potentially contributing to gastric injury.
  • Helicobacter pylori infection and cyclooxygenase inhibition are associated with gastric inflammation and injury.

Purpose of the Study:

  • To investigate whether MMP secretion by gastric epithelial cells contributes to gastric injury.
  • To determine the signaling pathways regulating MMP-1 and MMP-13 secretion in response to inflammatory stimuli and growth factors.
  • To explore the role of prostaglandins (PGEs) in regulating MMP secretion.

Main Methods:

  • Stimulation of gastric epithelial cells with tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and epidermal growth factor (EGF).
  • Analysis of MMP-1 and MMP-13 secretion.
  • Investigation of mitogen-activated protein kinase (MAPK) pathways (Erk and p38) involvement.
  • Assessment of protein synthesis requirements and prostaglandin (PGE) effects.

Main Results:

  • TNF-alpha, IL-1beta, and EGF stimulated MMP-1 secretion via Erk activation and protein synthesis.
  • TNF-alpha/IL-1beta stimulated MMP-13 secretion via p38, independent of Erk.
  • MMP-13 secretion was faster than MMP-1 secretion.
  • Prostaglandins (PGEs) differentially regulated MMP-1 secretion in a context-dependent manner, affecting Erk activation.

Conclusions:

  • MMP-1 and MMP-13 secretion are differentially regulated by distinct MAPK pathways in gastric epithelial cells.
  • These findings suggest mechanisms by which H. pylori infection and cyclooxygenase inhibition may promote gastric ulcerogenesis through epithelial MMP secretion.
  • E prostaglandins exert context-dependent effects on gastric cell responses and MMP secretion.

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