Abstract | BACKGROUND AND AIMS: METHODS: RESULTS: Levels of activin transcripts in the colon during the acute phase of TNBS colitis were up-regulated. Epithelial cells, infiltrating macrophages (Mvarphi), and endothelial cells produced excess activin betaA. Pretreatment with follistatin increased the survival rate of mice with TNBS colitis from 33% to 82% and decreased the plasma levels of IL-6 and amyloid A. Administration of follistatin also reduced the histologic score and tissue myeloperoxidase activity in established TNBS and DSS colitis and reduced the severity of the colitis in IL-10 -/- mice. Based on results obtained from 3 mouse models and from in vitro experiments, follistatin promoted the proliferation of colonic epithelial cells. CONCLUSIONS: Neutralization of activins by follistatin promoted epithelial cell division and tissue repair, clearly suggesting a treatment modality for intestinal inflammation.
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Authors | Taeko Dohi, Chieko Ejima, Rie Kato, Yuki I Kawamura, Rei Kawashima, Noriko Mizutani, Yoshiaki Tabuchi, Itaru Kojima |
Journal | Gastroenterology
(Gastroenterology)
Vol. 128
Issue 2
Pg. 411-23
(Feb 2005)
ISSN: 0016-5085 [Print] United States |
PMID | 15685552
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Follistatin
- RNA, Messenger
- Trinitrobenzenesulfonic Acid
- Peroxidase
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Topics |
- Animals
- Colitis
(chemically induced, drug therapy)
- Colonic Diseases
(drug therapy)
- Female
- Follistatin
(therapeutic use)
- Inflammation
(drug therapy)
- Intestinal Mucosa
(drug effects, pathology)
- Mice
- Mice, Inbred BALB C
- Peroxidase
(metabolism)
- RNA, Messenger
(genetics)
- Reverse Transcriptase Polymerase Chain Reaction
- Trinitrobenzenesulfonic Acid
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