PMID- 22479555
OWN - NLM
STAT- MEDLINE
DCOM- 20121105
LR  - 20211203
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 7
IP  - 3
DP  - 2012
TI  - Unlike for human monocytes after LPS activation, release of TNF-alpha by THP-1 cells 
      is produced by a TACE catalytically different from constitutive TACE.
PG  - e34184
LID - 10.1371/journal.pone.0034184 [doi]
LID - e34184
AB  - BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) is a pro-inflammatory cytokine 
      today identified as a key mediator of several chronic inflammatory diseases. 
      TNF-alpha, initially synthesized as a membrane-anchored precursor (pro-TNF-alpha), is 
      processed by proteolytic cleavage to generate the secreted mature form. TNF-alpha 
      converting enzyme (TACE) is currently the first and single protease described as 
      responsible for the inducible release of soluble TNF-alpha. METHODOLOGY/PRINCIPAL 
      FINDINGS: Here, we demonstrated the presence on THP-1 cells as on human monocytes 
      of a constitutive proteolytical activity able to cleave pro-TNF-alpha. Revelation of 
      the cell surface TACE protein expression confirmed that the observed catalytic 
      activity is due to TACE. However, further studies using effective and innovative 
      TNF-alpha inhibitors, as well as a highly selective TACE inhibitor, support the 
      presence of a catalytically different sheddase activity on LPS activated THP-1 
      cells. It appears that this catalytically different TACE protease activity might 
      have a significant contribution to TNF-alpha release in LPS activated THP-1 cells, by 
      contrast to human monocytes where the TACE activity remains catalytically 
      unchanged even after LPS activation. CONCLUSIONS/SIGNIFICANCE: On the surface of 
      LPS activated THP-1 cells we identified a releasing TNF-alpha activity, catalytically 
      different from the sheddase activity observed on human monocytes from healthy 
      donors. This catalytically-modified TACE activity is different from the 
      constitutive shedding activity and appears only upon stimulation by LPS.
FAU - Moreira-Tabaka, Helena
AU  - Moreira-Tabaka H
AD  - Laboratoire d'Innovation Therapeutique, UMR 7200, Faculte de Pharmacie, 
      Universite de Strasbourg, Illkirch, France. heltab@basmed.am.wroc.pl
FAU - Peluso, Jean
AU  - Peluso J
FAU - Vonesch, Jean-Luc
AU  - Vonesch JL
FAU - Hentsch, Didier
AU  - Hentsch D
FAU - Kessler, Pascal
AU  - Kessler P
FAU - Reimund, Jean-Marie
AU  - Reimund JM
FAU - Dumont, Serge
AU  - Dumont S
FAU - Muller, Christian D
AU  - Muller CD
LA  - eng
PT  - Journal Article
DEP - 20120330
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 
      (2-(1-(hydroxycarbamoyl)-4-phenyl-3-butenyl)-2'-isobutyl-2'-(methanesulfonyl)-4-methylvalerohydrazide)
RN  - 0 (Benzoquinones)
RN  - 0 (Hydroxamic Acids)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Pentacyclic Triterpenes)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Sulfonamides)
RN  - 0 (Triterpenes)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.- (Peptide Hydrolases)
RN  - EC 3.4.24.- (ADAM Proteins)
RN  - EC 3.4.24.86 (ADAM17 Protein)
RN  - EC 3.4.24.86 (ADAM17 protein, human)
RN  - EC 3.4.24.86 (Adam17 protein, mouse)
RN  - L8GG98663L (celastrol)
RN  - O60IE26NUF (thymoquinone)
SB  - IM
MH  - ADAM Proteins/*metabolism
MH  - ADAM17 Protein
MH  - Animals
MH  - Benzoquinones/pharmacology
MH  - Cell Line
MH  - Cell Membrane/metabolism
MH  - Chronic Disease
MH  - Enzyme-Linked Immunosorbent Assay/methods
MH  - Flow Cytometry/methods
MH  - Humans
MH  - Hydroxamic Acids/pharmacology
MH  - Inflammation
MH  - Inhibitory Concentration 50
MH  - Lipopolysaccharides/*metabolism
MH  - Mice
MH  - Microscopy, Confocal/methods
MH  - Monocytes/*cytology
MH  - Pentacyclic Triterpenes
MH  - Peptide Hydrolases/metabolism
MH  - Recombinant Proteins/metabolism
MH  - Sulfonamides/pharmacology
MH  - Triterpenes/pharmacology
MH  - Tumor Necrosis Factor-alpha/*metabolism
PMC - PMC3316627
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2012/04/06 06:00
MHDA- 2012/11/06 06:00
PMCR- 2012/03/30
CRDT- 2012/04/06 06:00
PHST- 2011/05/24 00:00 [received]
PHST- 2012/02/28 00:00 [accepted]
PHST- 2012/04/06 06:00 [entrez]
PHST- 2012/04/06 06:00 [pubmed]
PHST- 2012/11/06 06:00 [medline]
PHST- 2012/03/30 00:00 [pmc-release]
AID - PONE-D-11-09370 [pii]
AID - 10.1371/journal.pone.0034184 [doi]
PST - ppublish
SO  - PLoS One. 2012;7(3):e34184. doi: 10.1371/journal.pone.0034184. Epub 2012 Mar 30.