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Potential Role of the 15kDA Selenoprotein in Colorectal Inflammation
Author(s) -
Tsuji Petra,
Carlson Bradley,
Canter Jessica,
Onyewu Chukwuka,
Saylor Charlotte,
Tobe Ryuta,
Seifried Harold,
Yu Yunkai,
Cao Liang,
Gladyshev Vadim,
Davis Cindy,
Hatfield Dolph
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.759.1
Subject(s) - selenoprotein , azoxymethane , immune system , inflammation , gene expression , biology , proinflammatory cytokine , microarray , colitis , carcinogenesis , gene , immunology , oxidative stress , biochemistry , catalase , glutathione peroxidase
Selenium (Se) exerts its mechanistic effects through incorporation into selenoproteins, many of which are involved in cell homeostasis. Previous results suggest 15kDa selenoprotein (Sep15) deficiency is protective against colon cancer. Currently, we are examining tissues of mice with ( +/+ ) and without ( ‐/‐ ) Sep15 in a dextran sulfate sodium (DSS) model of colitis. Microarray analyses of colon epithelia showed that mRNA expression of seven top up‐regulated genes in Sep15 ‐/‐ mice compared to controls were changed regardless of DSS treatment. These genes are known to be involved in immune and pro‐inflammatory responses. Quantitative RT‐PCR indicated that mRNA expression of β‐catenin, an integral gene in colon tumorigenesis, was significantly increased in DSS treated Sep15 ‐/‐ mice compared to controls. Furthermore, serum interferon‐γ and interleukin‐6 levels were increased in Sep15 ‐/‐ mice under Se‐deficient conditions compared to Sep15 +/+ controls, regardless of DSS treatment. Thus, our preliminary analyses indicate that Sep15 is involved in the regulation of inflammatory responses. The contribution of other cytokines and of the gut microbiome are currently being assessed. Funding: NCI Intramural support; NIH CA080946 (VNG); Office of Dietary Supplements; Towson University Jess & Mildred Fisher Endowed Chair (PAT)