Increased Immunoreactivity of Cathepsins in the Rat Esophagus under Chronic Acid Reflux Esophagitis

Author:

Suyama Masayuki1234,Koike Masato1234,Asaoka Daisuke1234,Mori Hiroki1234,Oguro Masako1234,Ueno Takashi1234,Nagahara Akihito1234,Watanabe Sumio1234,Uchiyama Yasuo1234

Affiliation:

1. Department of Gastroenterology (MS, DA, HM, MO, AN, SW), Juntendo University School of Medicine, Tokyo, Japan

2. Department of Cell Biology and Neuroscience (MK,YU), Juntendo University School of Medicine, Tokyo, Japan

3. Center for Biomedical Research Resources (TU), Juntendo University Graduate School of Medicine, Tokyo, Japan

4. Department of Cellular and Molecular Neuropathology (YU), Juntendo University Graduate School of Medicine, Tokyo, Japan

Abstract

We have designed a stable rat chronic acid reflux esophagitis (RE) model. In gastrointestinal lesions, several lysosomal cathepsins are known to participate in epithelial permeability in cell-cell connections, such as tight junctions in ulcerative colitis. However, very few studies have focused on the distribution of cathepsins in the esophageal multilayer squamous epithelium. Therefore to clarify the role of cathepsins in RE, we investigated their immunohistological localization in the esophageal epithelium under normal conditions and after RE. Of the cathepsins examined (cathepsins B, C, D, F, H, L, S, and X), granular immunoreactivity for cathepsins B, C, D and L was observed in the control esophageal epithelia; although, their distribution differed depending on the enzyme examined. In the RE model, immunoreactivity of these cathepsins was increased in esophageal epithelial cells and activated macrophages. The immunoreactivity for cathepsins F, H, S and X was barely detectable in the control esophageal epithelium. However, in the RE model, we noticed a slight increase in the expression of cathepsins H and X in the epithelial cells. Furthermore, activated macrophages of the RE model possessed intense immunoreactivity for these cathepsins, which may have been related to esophageal inflammatory mechanisms.

Publisher

SAGE Publications

Subject

Histology,Anatomy

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