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Post-transcriptional regulation of meprin α by the RNA-binding proteins Hu antigen R (HuR) and tristetraprolin (TTP)

Alanna N Roff1, Ronaldo P Panganiban, Judith S Bond

  • 1Department of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.

The Journal of Biological Chemistry
|December 28, 2012
PubMed

Insights

Inflammatory bowel disease patients have lower meprin alpha levels. This study reveals how inflammation reduces meprin alpha by destabilizing its transcript via tristetraprolin, clarifying meprin

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Immunology

Background:

  • Meprins are proteases linked to inflammatory bowel disease (IBD).
  • IBD patients exhibit reduced colonic meprin alpha expression.
  • Mechanisms regulating meprin alpha under inflammation are poorly understood.

Purpose of the Study:

  • To investigate the post-transcriptional regulation of human meprin alpha expression.
  • To elucidate the role of inflammatory stimuli in meprin alpha regulation.

Main Methods:

  • Analysis of meprin alpha transcript stability.
  • Investigation of RNA-binding proteins Hu antigen R and tristetraprolin.
  • Use of phorbol 12-myristate 13-acetate as an inflammatory stimulus.

Main Results:

  • The human meprin alpha transcript is stabilized by Hu antigen R at baseline.
  • Inflammatory stimulus (phorbol 12-myristate 13-acetate) induces tristetraprolin.
  • Tristetraprolin binds the MEP1A 3'-UTR, destabilizing the meprin alpha transcript at a distinct site from Hu antigen R.

Conclusions:

  • This study identifies a novel mechanism for post-transcriptional regulation of meprin alpha.
  • Tristetraprolin-mediated destabilization of meprin alpha transcript is induced by inflammation.
  • Findings clarify the role of meprins in inflammatory responses and IBD pathogenesis.

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