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Increased Expression of Serum‐ and Glucocorticoid‐regulated Kinase‐1 in the Duodenal Mucosa of Children With Coeliac Disease
Author(s) -
Szebeni Beáta,
Vannay Ádám,
Sziksz Erna,
Prókai Ágnes,
Cseh Áron,
Veres Gábor,
Dezsőfi Antal,
Győrffy Hajnalka,
Szabó IR Korponay,
Arató András
Publication year - 2010
Publication title -
journal of pediatric gastroenterology and nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 131
eISSN - 1536-4801
pISSN - 0277-2116
DOI - 10.1097/mpg.0b013e3181b47608
Subject(s) - sgk1 , intraepithelial lymphocyte , enterocyte , western blot , medicine , intestinal mucosa , biopsy , kinase , messenger rna , endocrinology , coeliac disease , apoptosis , microbiology and biotechnology , pathology , biology , glucocorticoid , small intestine , epithelium , gene , biochemistry , disease
Objectives: Enterocyte apoptosis induced by activated intraepithelial lymphocytes is increased in coeliac disease (CD). Serum‐ and glucocorticoid‐regulated kinase‐1 (SGK1) is a serine/threonine protein kinase that may inhibit apoptosis and compensate for the excessive death of surface epithelial cells. The significance of SGK1 in CD is elusive so far. The aim of this study was to characterise the expression and localisation of SGK1 in duodenal biopsy samples taken from children with untreated CD, children with treated CD, and controls. Patients and Methods: Duodenal biopsy specimens were collected from 16 children with untreated CD, 9 children with treated CD, and 10 controls. The mRNA expression of SGK1 was determined by real‐time reverse transcription‐polymerase chain reaction. SGK1 and phosphorylated (P)‐SGK1 protein levels and their localisation were determined by Western blot and immunfluorescent staining, respectively. Results: We found increased SGK1‐mRNA expression as well as higher SGK1 and P‐SGK1 protein levels in the duodenal mucosa of children with untreated CD compared with controls. In the duodenal mucosa of children with treated CD, SGK1‐mRNA expression was decreased and SGK1 and P‐SGK1 protein levels were lower than in untreated CD. SGK1 and P‐SGK1 staining intensity was stronger in duodenal villous enterocytes of children with untreated CD compared with treated CD. Conclusions: Our results of increased expression of SGK1 in untreated CD may suggest its contribution to the enterocyte survival in this disease.

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