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Effect of Pre‐adipocyte and Differentiated Adipocyte Conditioned Media on Galectin‐3 Expression in Mouse Intestinal Epithelial Cell
Author(s) -
Kim JonSang,
Garcia Annalene,
SEO Jiyeon,
LIM Ji Sun,
Park Jia,
Nam Dae Hwan,
Sung MiKyung
Publication year - 2010
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.24.1_supplement.541.17
Subject(s) - adipocyte , inflammation , carcinogenesis , downregulation and upregulation , galectin 3 , western blot , tumor necrosis factor alpha , endocrinology , biology , medicine , cancer research , chemistry , adipose tissue , microbiology and biotechnology , cancer , immunology , biochemistry , gene
We hypothesized that obesity cause inflammation which, in turn, promotes colon carcinogenesis. To test the hypothesis mouse intestinal IEC‐6 cells were incubated in the presence of preconditioned media collected from culturing LPS‐stimulated macrophage, followed by comparing protein expression profile with control cells. The proteomic analysis revealed 45 differentially regulated proteins in mouse intestinal IEC‐6 cells under the inflammation‐mimicking condition. Among others, galectin‐3, a beta‐galactoside‐binding protein, was up‐regulated. Galectin‐3 has been reported to play anti‐apoptotic role in tumor progression and metastasis, and its over‐expression has been observed in several types of cancer such as colon cancer. In order to determine relationship between obesity‐induced inflammation and colon carcinogenesis, conditioned media (CM) from LPS‐stimulated or non‐stimulated 3T3‐L1 pre‐adipocytes or differentiated adipocytes were utilized to induce inflammation in IEC‐6 cells. Nitric oxide (NO) level was determined using Griess method and galectin‐3 expression was analyzed by western blot. Results showed enhanced generation of NO and upregulation of galectin‐3 in both LPS‐stimulated pre‐adipocyte and adipocyte. The increased expression of galectin‐3 in IEC cells might be caused by high levels of TNF‐alpha and IL‐6 in CM.