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J Gastroenterol Hepatol. 2016 Nov 21. doi: 10.1111/jgh.13664. [Epub ahead of print]

PRDX2 up-regulation in inflammatory bowel disease: friend or foe?

Author information

  • 1Laboratory of Genetics and Molecular pathologies, Faculty of Medicine and Pharmacy of Casablanca, Hassan II University, Morocco.
  • 2Laboratory of Thrombosis and Hemostasis, Montreal Heart Institute, Montreal, Quebec, Canada.
  • 3Laboratory of Physiology and Molecular Genetics, Faculty of Sciences Aïn Chock, Hassan II University, Casablanca, Morocco.
  • 4Gastroenterology Department, CHU IbnRochd, Casablanca, Morocco.
  • 5Instituto de Parasitología y Biomedicina López-Neyra, Consejo Superior de Investigaciones Científicas, Granada, Spain.



Inflammatory bowel diseases (IBD) are chronic multi-factorial inflammatory disorders. Accumulating investigations have provided compelling evidence that describe the interplay of a complex genetic landscape and inappropriate inflammatory response to intestinal microbes in disease etiopathogenesis, but still pose challenges in diagnostic practices.


In this study, comparative proteomic analysis was conducted to identify disease specific proteins underlying IBD pathogenetic mechanisms. Total blood proteins of the IBD patients and healthy subjects were analyzed with one-dimensional electrophoresis; differentially expressed bands were excised and subjected to MALDI-TOF/TOF-MS/MS along with nLC-ESI-MS/MS analysis. Presence of glycosylation, hydroxylation and phosphorylation post-translational modifications was further investigated by immunoprecipitation.


PRDX2 and Hemoglobin-subunits proteins, which are closely involved in the response to oxidative stress, were identified. PRDX2 was selected for further validation using Western blot and RT-PCR. PRDX2 over-expression was restricted to the protein level within the membrane fraction. Immunoprecipitation identified PRDX2 to be post-translationally glycosylated and phosphorylated.


Our findings demonstrate the implication of PRDX2 in IBD. Future studies are required to establish its functional role and to determine the clinical utility.


Hemoglobin-subunits; IBD; PRDX2

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