Presenting Author: Arong Gaowa
, Assistant Prof. at Mie Univ.
Abstract:
Intestinal fibrosis, a common complication of intestinal bowel disease and is defined as an excessive deposition of extracellular matrix protein in the intestinal wall. Rosiglitazone, a PPAR-γ agonist, exerts anti-fibrotic effect in several organ fibrosis; however, its inhibitory effect on intestinal fibrosis is still not completely understood. Here, we investigated the inhibitory effects of rosiglitazone on fibrotic gene expression using TGFβ1 induced intestinal fibrosis model. Intestinal organoids were treated with TGFβ1 alone (2 ng/mL) or TGFβ1 plus rosiglitazone (50 uM) for 24 hours. Markers of fibrogenesis, including collagens and fibronectin were evaluated by measuring mRNA level using RT-PCR, and protein level by immunofluorescence or Western blotting. Signaling pathways involved in fibrosis were characterized by Western blotting analysis of cell lysates using indicated antibodies. We found that rosiglitazone significantly suppressed TGFβ1-induced expression of profibrogenic genes (collagen and fibronectin), epithelial to mesenchymal transition and cytokines production in intestinal fibrosis model. Furthermore, it was found that rosiglitazone inhibited the phosphorylation of Smad2/3 and Erk1/2. Taken together, these findings indicate that rosiglitazone exerts potent anti-fibrotic effect in TGFβ1 induced intestinal fibrosis via Smad- and non-Smad pathway.
Rosiglitazone, a PPAR-γ agonist inhibits extracellular matrix production in TGFβ1 induced intestinal fibrosis.
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Poster
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Date: May 5 Presentation Time: 03:15 PM to 04:30 PM Room: Exhibit Hall F1