Early methyl donor deficiency produces severe gastritis in mothers and offspring through N-homocysteinylation of cytoskeleton proteins, cellular stress, and inflammation.

Date publication

juin 2013

Auteurs

Membres identifiés du Cancéropôle Est :
Pr GUEANT Jean-Louis

Tous les auteurs :
Bossenmeyer-Pourie C, Pourie G, Koziel V, Helle D, Jeannesson E, Gueant JL, Beck B

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/23401564

Résumé

We examined the gastric mucosa structure and inflammatory status in control well-nourished Wistar dams and in Wistar dams deprived of choline, folate, and vitamin B12 during gestation and suckling periods, and in their offspring just before birth and at weaning. In this model of methyl donor deficiency (MDD), structural protein (E-cadherin and actin) N-homocysteinylation was measured through immunoprecipitation and proximity ligation assays. Cellular stress, inflammation, and apoptosis were estimated by the analysis of the NF-kappaB pathway, and the expression of superoxide dismutase, cyclooxygenase-2, tumor necrosis factor alpha, caspases 3 and 9, and TUNEL assay. Aberrant gastric mucosa formation and signs of surface layer erosion were detected in MDD fetuses and weanlings. E-cadherin and actin were N-homocysteinylated (+215 and +249% vs. controls, respectively; P

Référence

FASEB J. 2013 Jun;27(6):2185-97