PMID- 11334117
OWN - NLM
STAT- MEDLINE
DCOM- 20010920
LR  - 20190822
IS  - 0903-1936 (Print)
IS  - 0903-1936 (Linking)
VI  - 17
IP  - 2
DP  - 2001 Feb
TI  - Upregulation of Fas-signalling molecules in lung epithelial cells from patients 
      with idiopathic pulmonary fibrosis.
PG  - 180-9
AB  - The caspase cascade is an executioner of apoptosis, mediated by Fas. 
      Fas-associating protein with death domain (FADD) interacts with Fas and initiates 
      apoptosis through activating caspase-8. It has previously been demonstrated that 
      the Fas-Fas ligand pathway may be involved in the pathophysiology of idiopathic 
      pulmonary fibrosis (IPF). The aim of this study was to investigate Fas-signalling 
      molecules in epithelial cells in IPF. The immunohistochemistry for FADD and 
      caspase-1 and -3 and terminal deoxynucleotidyl transferase-mediated 
      deoxyuridinetriphosphate nick endlabelling (TUNEL) methods were performed in lung 
      tissues from 10 patients with IPF obtained by thoracoscopic biopsy and in seven 
      normal lung parenchyma specimens. The induction of caspases expression and 
      activation by Fas-ligation on lung epithelial cell line A549 was also 
      investigated. The immunoreactivity grade for FADD and caspase-1 and -3, and 
      positive signals for TUNEL were significantly increased in epithelial cells of 
      IPF compared with controls. Fas-ligation induced upregulation of caspase-1 and -3 
      expression in the nucleus and cytoplasm in A549 cells. Procaspase-1, -3, and -8 
      were activated in apoptotic cells, but not in viable cells. Although direct 
      measurement of the caspase activity in lung epithelial cells of idiopathic 
      pulmonary fibrosis could not be made, these results suggest that the 
      Fas-signalling pathway is upregulated in lung epithelial cells of idiopathic 
      pulmonary fibrosis.
FAU - Maeyama, T
AU  - Maeyama T
AD  - Research Institute for Diseases of the Chest, Graduate School of Medical 
      Sciences, Kyushu University, Fukuoka, Japan.
FAU - Kuwano, K
AU  - Kuwano K
FAU - Kawasaki, M
AU  - Kawasaki M
FAU - Kunitake, R
AU  - Kunitake R
FAU - Hagimoto, N
AU  - Hagimoto N
FAU - Matsuba, T
AU  - Matsuba T
FAU - Yoshimi, M
AU  - Yoshimi M
FAU - Inoshima, I
AU  - Inoshima I
FAU - Yoshida, K
AU  - Yoshida K
FAU - Hara, N
AU  - Hara N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Eur Respir J
JT  - The European respiratory journal
JID - 8803460
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Carrier Proteins)
RN  - 0 (FADD protein, human)
RN  - 0 (Fas-Associated Death Domain Protein)
RN  - EC 3.4.22.- (CASP3 protein, human)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspases)
RN  - EC 3.4.22.36 (Caspase 1)
SB  - IM
MH  - *Adaptor Proteins, Signal Transducing
MH  - Aged
MH  - *Apoptosis
MH  - Blotting, Western
MH  - Carrier Proteins/*analysis
MH  - Caspase 1/analysis
MH  - Caspase 3
MH  - Caspases/analysis
MH  - Cell Line
MH  - Enzyme Activation
MH  - Epithelial Cells/metabolism
MH  - Fas-Associated Death Domain Protein
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Nick-End Labeling
MH  - Lung/*metabolism/pathology
MH  - Male
MH  - Middle Aged
MH  - Pulmonary Fibrosis/*metabolism/pathology
MH  - *Signal Transduction
MH  - Up-Regulation
EDAT- 2001/05/04 10:00
MHDA- 2001/09/21 10:01
CRDT- 2001/05/04 10:00
PHST- 2001/05/04 10:00 [pubmed]
PHST- 2001/09/21 10:01 [medline]
PHST- 2001/05/04 10:00 [entrez]
AID - 10.1183/09031936.01.17201800 [doi]
PST - ppublish
SO  - Eur Respir J. 2001 Feb;17(2):180-9. doi: 10.1183/09031936.01.17201800.