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Expression of Transforming Growth Factor-beta and Its Receptors during Acetic Acid-induced Duodenal Ulcer Healing in Rats.
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Original Article Expression of Transforming Growth Factor-beta and Its Receptors during Acetic Acid-induced Duodenal Ulcer Healing in Rats.
Kyu Yun Jang, Han Sang Yoon, Ki Hoon Yu, Myung Ja Chung, Dong Geun Lee, Jae Kang Myoung
Journal of Pathology and Translational Medicine 2003;37(2):108-114
DOI: https://doi.org/
Department of Pathology, Chonbuk National University Medical School, Chonju, Korea. mjkang@moak.chonbuk.ac.kr
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BACKGROUND
Many works have been written about the transforming growth factor-beta 1 (TGF-beta1) which is closely associated with fibrosis in the inflammatory conditions of different organs. TGF-beta1 exerts its biological effects by interacting with specific cell surface receptors, namely, transforming growth factor-beta receptor type I and II (TGFbetaRI and TGFbetaRII).
METHODS
To investigate the temporal expressions and localizations of TGF-beta1, TGFRbetaI, and TGFbetaRII in acetic acid-induced duodenal ulcerated tissues, we performed in situ hybridization and immunohistochemical techniques.
RESULTS
Under in situ hybridization, TGF-beta1, TGFbetaRI, and TGFbetaRII mRNA signals increased in the experimental groups (1, 3, 7, and 14 day groups) compared to those of the control group. The signals on day 14 decreased slightly compared to those of days 1, 3, and 7, but they were higher than those of the control group. Under immunohistochemical study, TGF-beta1, TGFbetaRI, and TGFbetaRII were localized in the mucosal epithelial cells and in the macrophages, vascular endothelial cells, and fibroblasts of the lamina propria and granulation tissue. As in the case of the in situ hybridization, it revealed that the expression of three proteins increased in the experimental groups compared to that of the control group. The expression on day 14 decreased compared to those of days 1, 3, and 7, but it was more intense than that of the control group.
CONCLUSIONS
This study suggests that TGF-beta1, TGFbetaRI, and TGFbetaRII contribute to the early stage healing of duodenal ulcer.

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