PMID- 17492827
OWN - NLM
STAT- MEDLINE
DCOM- 20070629
LR  - 20131121
IS  - 0022-3417 (Print)
IS  - 0022-3417 (Linking)
VI  - 212
IP  - 2
DP  - 2007 Jun
TI  - Antiapoptotic effect of found in inflammatory zone (FIZZ)1 on mouse lung 
      fibroblasts.
PG  - 180-7
AB  - Myofibroblasts play an essential role in the abnormal deposition of extracellular 
      matrix in pulmonary fibrosis. The presence or prolonged survival of these cells 
      may be a key factor in the pathogenesis of progressive pulmonary fibrosis. Found 
      in inflammatory zone (FIZZ)1 can induce myofibroblast differentiation and has an 
      antiapoptotic effect on embryonic lung explant cultures. In this study, we 
      investigated whether FIZZ1 also has an antiapoptotic effect on mouse lung 
      fibroblasts (MLFs). Cells were treated with FIZZ1 for 24 h and then apoptosis was 
      induced by TNFalpha in the presence of cycloheximide (CHX). FIZZ1 exhibited an 
      antiapoptotic effect in MLFs, as assessed by flow cytometric analysis and TUNEL 
      staining. Moreover, the cell number was higher in the FIZZ1-treated group 
      relative to the non-treated control group after treatment with TNFalpha and CHX. 
      FIZZ1 treatment also inhibited the apoptotic agent-induced activities of 
      caspase-3 and caspase-8. Examination of potential signalling pathways revealed 
      that FIZZ1 induced rapid phosphorylation of ERK-1/2, while PD98059, a MEK/ERK 
      inhibitor, markedly induced activation of caspase-3. This anti-apoptotic effect 
      of FIZZ1 was associated with induction of myofibroblast differentiation in 
      response to FIZZ1 stimulation. Taken together, these findings suggest that FIZZ1 
      is involved in pulmonary fibrosis through both induction of myofibroblast 
      differentiation and increased or prolonged survival of myofibroblasts. This 
      effect of FIZZ1 was mediated by inhibition of caspase-3 and -8, with involvement 
      of the ERK pathway.
CI  - Copyright 2007 Pathological Society of Great Britain and Ireland. Published by 
      John Wiley & Sons, Ltd.
FAU - Chung, M J
AU  - Chung MJ
AD  - Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 
      48109-2200, USA.
FAU - Liu, T
AU  - Liu T
FAU - Ullenbruch, M
AU  - Ullenbruch M
FAU - Phan, S H
AU  - Phan SH
LA  - eng
GR  - HL28737/HL/NHLBI NIH HHS/United States
GR  - HL31963/HL/NHLBI NIH HHS/United States
GR  - HL52285/HL/NHLBI NIH HHS/United States
GR  - HL77297/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - England
TA  - J Pathol
JT  - The Journal of pathology
JID - 0204634
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Protein Synthesis Inhibitors)
RN  - 0 (Proteins)
RN  - 0 (Retnla protein, mouse)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - 98600C0908 (Cycloheximide)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspase 8)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects/immunology
MH  - Caspase 3/metabolism
MH  - Caspase 8/metabolism
MH  - Cell Differentiation/drug effects
MH  - Cycloheximide/pharmacology
MH  - Enzyme Activation/drug effects
MH  - Female
MH  - Fibroblasts/*drug effects/physiology
MH  - Intercellular Signaling Peptides and Proteins
MH  - Lung/*drug effects/physiology
MH  - MAP Kinase Signaling System/drug effects
MH  - Mice
MH  - Mice, Inbred CBA
MH  - Mitogen-Activated Protein Kinase 3/metabolism
MH  - Nerve Growth Factor/pharmacology
MH  - Protein Synthesis Inhibitors/pharmacology
MH  - Proteins/*pharmacology
MH  - Proto-Oncogene Proteins c-akt/analysis
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 2007/05/12 09:00
MHDA- 2007/06/30 09:00
CRDT- 2007/05/12 09:00
PHST- 2007/05/12 09:00 [pubmed]
PHST- 2007/06/30 09:00 [medline]
PHST- 2007/05/12 09:00 [entrez]
AID - 10.1002/path.2161 [doi]
PST - ppublish
SO  - J Pathol. 2007 Jun;212(2):180-7. doi: 10.1002/path.2161.