Fas ligand and Fas receptor are coexpressed in normal human esophageal epithelium: a potential mechanism of apoptotic epithelial turnover

Citation
Mw. Bennett et al., Fas ligand and Fas receptor are coexpressed in normal human esophageal epithelium: a potential mechanism of apoptotic epithelial turnover, DIS ESOPHAG, 12(2), 1999, pp. 90-98
Citations number
32
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
DISEASES OF THE ESOPHAGUS
ISSN journal
11208694 → ACNP
Volume
12
Issue
2
Year of publication
1999
Pages
90 - 98
Database
ISI
SICI code
1120-8694(1999)12:2<90:FLAFRA>2.0.ZU;2-O
Abstract
Fas (CD95/Apo-1) receptor (FasR) is a cell-surface receptor that mediates a poptotic cell death upon triggering by Fas ligand (FasL), We sought to dete rmine whether normal human esophageal epithelial cells express Fast and/or FasR and whether their localization is consistent with a role in the turnov er of normal esophageal epithelium. Normal esophageal epithelium was immuno histochemically positive for Fast in upper prickle cell layers and in matur e squamous cells, but the proliferative basal layer was negative, Fast mRNA was detected in the same epithelial cell layers by in situ hybridization, Go-Localization of Fast mRNA and protein therefore confirmed that Fast expr ession is induced in esophageal epithelial cells as they reach terminal dif ferentiation, FasR was immunohistochemically detected throughout the esopha geal epithelium, Positive TUNEL (terminal deoxynucleotidyl transferase (TdT )-mediated dUTP nick end-labeling) staining confirmed cell death of the Fas t and FasR coexpressing mature epithelial cells. CD45-positive immunocytes were notably absent from Fast-expressing upper epithelial layers, The findi ngs are consistent with a contributory role for Fas-mediated autocrine suic ide or paracrine fratricide in the apoptotic turnover of normal esophageal epithelium.