TY  - JOUR
  - Bennett, M. W.,O'Connell, J.,O'Sullivan, G. C.,Roche, D.,Brady, C.,Collins, J. K.,Shanahan, F.
  - 1999
  - Unknown
  - Diseases of the Esophagus
  - Fas ligand and Fas receptor are coexpressed in normal human esophageal epithelium: a potential mechanism of apoptotic epithelial turnover
  - Validated
  - ()
  - 12
  - 2
  - 90
  - 98
  - Fas (CD95/Apo-1) receptor (FasR) is a cell-surface receptor that mediates apoptotic cell death upon triggering by Fas ligand (FasL), We sought to determine whether normal human esophageal epithelial cells express Fast and/or FasR and whether their localization is consistent with a role in the turnover of normal esophageal epithelium. Normal esophageal epithelium was immunohistochemically positive for Fast in upper prickle cell layers and in mature 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 expression is induced in esophageal epithelial cells as they reach terminal differentiation, FasR was immunohistochemically detected throughout the esophageal epithelium, Positive TUNEL (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling) staining confirmed cell death of the Fast and FasR coexpressing mature epithelial cells. CD45-positive immunocytes were notably absent from Fast-expressing upper epithelial layers, The findings are consistent with a contributory role for Fas-mediated autocrine suicide or paracrine fratricide in the apoptotic turnover of normal esophageal epithelium.Fas (CD95/Apo-1) receptor (FasR) is a cell-surface receptor that mediates apoptotic cell death upon triggering by Fas ligand (FasL), We sought to determine whether normal human esophageal epithelial cells express Fast and/or FasR and whether their localization is consistent with a role in the turnover of normal esophageal epithelium. Normal esophageal epithelium was immunohistochemically positive for Fast in upper prickle cell layers and in mature 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 expression is induced in esophageal epithelial cells as they reach terminal differentiation, FasR was immunohistochemically detected throughout the esophageal epithelium, Positive TUNEL (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling) staining confirmed cell death of the Fast and FasR coexpressing mature epithelial cells. CD45-positive immunocytes were notably absent from Fast-expressing upper epithelial layers, The findings are consistent with a contributory role for Fas-mediated autocrine suicide or paracrine fratricide in the apoptotic turnover of normal esophageal epithelium.
  - 1120-86941120-8694
  - ://WOS:000083699700002://WOS:000083699700002
DA  - 1999/NaN
ER  - 

@article{V235379814,
   = {Bennett,  M. W. and O'Connell,  J. and O'Sullivan,  G. C. and Roche,  D. and Brady,  C. and Collins,  J. K. and Shanahan,  F. },
   = {1999},
   = {Unknown},
   = {Diseases of the Esophagus},
   = {Fas ligand and Fas receptor are coexpressed in normal human esophageal epithelium: a potential mechanism of apoptotic epithelial turnover},
   = {Validated},
   = {()},
   = {12},
   = {2},
  pages = {90--98},
   = {{Fas (CD95/Apo-1) receptor (FasR) is a cell-surface receptor that mediates apoptotic cell death upon triggering by Fas ligand (FasL), We sought to determine whether normal human esophageal epithelial cells express Fast and/or FasR and whether their localization is consistent with a role in the turnover of normal esophageal epithelium. Normal esophageal epithelium was immunohistochemically positive for Fast in upper prickle cell layers and in mature 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 expression is induced in esophageal epithelial cells as they reach terminal differentiation, FasR was immunohistochemically detected throughout the esophageal epithelium, Positive TUNEL (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling) staining confirmed cell death of the Fast and FasR coexpressing mature epithelial cells. CD45-positive immunocytes were notably absent from Fast-expressing upper epithelial layers, The findings are consistent with a contributory role for Fas-mediated autocrine suicide or paracrine fratricide in the apoptotic turnover of normal esophageal epithelium.Fas (CD95/Apo-1) receptor (FasR) is a cell-surface receptor that mediates apoptotic cell death upon triggering by Fas ligand (FasL), We sought to determine whether normal human esophageal epithelial cells express Fast and/or FasR and whether their localization is consistent with a role in the turnover of normal esophageal epithelium. Normal esophageal epithelium was immunohistochemically positive for Fast in upper prickle cell layers and in mature 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 expression is induced in esophageal epithelial cells as they reach terminal differentiation, FasR was immunohistochemically detected throughout the esophageal epithelium, Positive TUNEL (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling) staining confirmed cell death of the Fast and FasR coexpressing mature epithelial cells. CD45-positive immunocytes were notably absent from Fast-expressing upper epithelial layers, The findings are consistent with a contributory role for Fas-mediated autocrine suicide or paracrine fratricide in the apoptotic turnover of normal esophageal epithelium.}},
  issn = {1120-86941120-8694},
   = {://WOS:000083699700002://WOS:000083699700002},
  source = {IRIS}
}