PMID- 15333331
OWN - NLM
STAT- MEDLINE
DCOM- 20050408
LR  - 20191210
IS  - 1073-449X (Print)
IS  - 1073-449X (Linking)
VI  - 170
IP  - 11
DP  - 2004 Dec 1
TI  - Importance of tumor necrosis factor-alpha cleavage process in 
      post-transplantation lung injury in rats.
PG  - 1239-46
AB  - Tumor necrosis factor-alpha (TNF-alpha) has two forms with apparently different 
      biological activities: a membrane-associated form and a soluble form. 
      TNF-alpha-converting enzyme (TACE) mediates a cleavage of membrane-associated 
      TNF-alpha to induce its bioactive soluble form. We hypothesized that inhibition 
      of TACE might prevent TNF-alpha-induced tissue injury while preserving the 
      benefits of TNF-alpha. In this study, we evaluated the role of TACE in acute 
      inflammation using an inhibitor of the enzyme in a rat model of lung 
      transplantation. Inbred Lewis rats underwent left lung isotransplantation, and 
      the donor lungs were kept in Euro-Collins solution with or without the inhibitor. 
      After 6 hours of ischemia, the left lung was transplanted into the recipient rat 
      and reperfused for 4 hours. Inhibition of TACE significantly attenuated 
      endothelial and alveolar septal damage, as assessed by radiolabeled albumin 
      leakage after transplantation. The inhibition also attenuated neutrophil 
      accumulation in the alveolar space and other histopathologic findings, including 
      intercellular adhesion molecule-1 expression. In addition, significantly lower 
      levels of monocyte chemotactic protein-1, cytokine-induced neutrophil 
      chemoattractant-1, high mobility group box-1, and soluble epithelial cadherin and 
      decreased neutrophil elastase activity were observed in bronchoalveolar lavage 
      fluid from the rats treated with the inhibitor. We conclude that TACE mediates a 
      critical step in the development of post-transplantation lung injury.
FAU - Goto, Taichiro
AU  - Goto T
AD  - Department of Surgery, School of Medicine, Keio University, 35 Shinanomachi, 
      Shinjuku-ku, Tokyo 160-8582, Japan.
FAU - Ishizaka, Akitoshi
AU  - Ishizaka A
FAU - Kobayashi, Fujio
AU  - Kobayashi F
FAU - Kohno, Mitsutomo
AU  - Kohno M
FAU - Sawafuji, Makoto
AU  - Sawafuji M
FAU - Tasaka, Sadatomo
AU  - Tasaka S
FAU - Ikeda, Eiji
AU  - Ikeda E
FAU - Okada, Yasunori
AU  - Okada Y
FAU - Maruyama, Ikuro
AU  - Maruyama I
FAU - Kobayashi, Koichi
AU  - Kobayashi K
LA  - eng
PT  - Evaluation Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20040827
PL  - United States
TA  - Am J Respir Crit Care Med
JT  - American journal of respiratory and critical care medicine
JID - 9421642
RN  - 0 (Cadherins)
RN  - 0 (Chemokines)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (HMGB1 Protein)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.24.- (ADAM Proteins)
RN  - EC 3.4.24.- (Metalloendopeptidases)
RN  - EC 3.4.24.86 (ADAM17 Protein)
RN  - EC 3.4.24.86 (Adam17 protein, rat)
SB  - IM
MH  - ADAM Proteins
MH  - ADAM17 Protein
MH  - Animals
MH  - Bronchoalveolar Lavage Fluid/immunology
MH  - Cadherins/immunology
MH  - Chemokines/immunology
MH  - Enzyme Inhibitors/*therapeutic use
MH  - HMGB1 Protein/immunology
MH  - Lung Diseases/*immunology/prevention & control
MH  - Lung Transplantation/*adverse effects
MH  - Metalloendopeptidases/*antagonists & inhibitors
MH  - Models, Animal
MH  - Rats
MH  - Rats, Inbred Lew
MH  - Respiratory Mucosa/drug effects/immunology
MH  - Tumor Necrosis Factor-alpha/adverse effects/*metabolism
EDAT- 2004/08/31 05:00
MHDA- 2005/04/09 09:00
CRDT- 2004/08/31 05:00
PHST- 2004/08/31 05:00 [pubmed]
PHST- 2005/04/09 09:00 [medline]
PHST- 2004/08/31 05:00 [entrez]
AID - 200402-146OC [pii]
AID - 10.1164/rccm.200402-146OC [doi]
PST - ppublish
SO  - Am J Respir Crit Care Med. 2004 Dec 1;170(11):1239-46. doi: 
      10.1164/rccm.200402-146OC. Epub 2004 Aug 27.