PMID- 9848873
OWN - NLM
STAT- MEDLINE
DCOM- 19990107
LR  - 20190831
IS  - 1079-5642 (Print)
IS  - 1079-5642 (Linking)
VI  - 18
IP  - 12
DP  - 1998 Dec
TI  - Inhibition of tumor necrosis factor-alpha- and interleukin-1-induced endothelial 
      E-selectin expression by thiol-modifying agents.
PG  - 1829-37
AB  - The expression of endothelial-leukocyte adhesion molecules has been postulated to 
      be regulated by redox-sensitive events. Tumor necrosis factor-alpha (TNF-alpha)- 
      and interleukin-1 (IL-1)-induced E-selectin expression was analyzed after 
      pretreating human umbilical vein endothelial cells with different thiol-modifying 
      agents, ie, diamide, phenylarsine oxide, N-ethylmaleimide, and diethyl maleate. 
      E-selectin protein expression was quantified by indirect immunofluorescence. All 
      compounds suppressed the cytokine-induced E-selectin expression in a 
      concentration-dependent manner, whereas the antioxidant N-acetylcysteine showed 
      no effect. The inhibitory effect of diamide (100 micromol/L, 1 hour) was 
      reversible within 6 hours when the cells were allowed to recover before 
      application of cytokines. Reversibility was strongly delayed when cells were 
      deprived of glutathione by buthionine sulfoximine pretreatment. Glutathione 
      depletion alone did not influence cytokine-induced E-selectin expression. 
      Analysis of cellular glutathione status showed a 3-fold increase in oxidized 
      glutathione after diamide treatment. Monochlorobimane labeling also revealed a 
      decrease in total cellular thiols. During recovery, the glutathione status was 
      restored within 1 hour, whereas total thiol content and E-selectin expression 
      needed at least 6 hours to return to baseline. Complete inhibition of E-selectin 
      expression by the vicinal thiol blocker phenylarsine oxide (0.5 micromol/L) was 
      reversed by dithiols like dithiothreitol or dimercaptopropanol, but not by the 
      monothiol 2-mercaptoethanol. These data suggest that proteins with essential 
      thiols, most probably vicinal thiols. are involved in the IL-1- and 
      TNF-alpha-mediated induction of E-selectin. These thiols must be in the reduced 
      state; oxidation or other modification thereof attenuates or abolishes the cells' 
      response to the cytokines.
FAU - Friedrichs, B
AU  - Friedrichs B
AD  - German Institute of Human Nutrition Potsdam-Rehbrucke and the Institute of 
      Nutritional Science, University of Potsdam Potsdam-Rehbrucke, Germany.
FAU - Muller, C
AU  - Muller C
FAU - Brigelius-Flohe, R
AU  - Brigelius-Flohe R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arterioscler Thromb Vasc Biol
JT  - Arteriosclerosis, thrombosis, and vascular biology
JID - 9505803
RN  - 0 (Arsenicals)
RN  - 0 (E-Selectin)
RN  - 0 (Interleukin-1)
RN  - 0 (Sulfhydryl Compounds)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0HUR2WY345 (oxophenylarsine)
RN  - 5072-26-4 (Buthionine Sulfoximine)
RN  - GAN16C9B8O (Glutathione)
RN  - ULW86O013H (Glutathione Disulfide)
RN  - WYQ7N0BPYC (Acetylcysteine)
SB  - IM
MH  - Acetylcysteine/pharmacology
MH  - Arsenicals/pharmacology
MH  - Buthionine Sulfoximine/pharmacology
MH  - Cells, Cultured
MH  - E-Selectin/*biosynthesis
MH  - Endothelium, Vascular/*metabolism
MH  - Glutathione/analysis/physiology
MH  - Glutathione Disulfide/analysis
MH  - Humans
MH  - Interleukin-1/*pharmacology
MH  - Sulfhydryl Compounds/*physiology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1998/12/16 00:00
MHDA- 1998/12/16 00:01
CRDT- 1998/12/16 00:00
PHST- 1998/12/16 00:00 [pubmed]
PHST- 1998/12/16 00:01 [medline]
PHST- 1998/12/16 00:00 [entrez]
AID - 10.1161/01.atv.18.12.1829 [doi]
PST - ppublish
SO  - Arterioscler Thromb Vasc Biol. 1998 Dec;18(12):1829-37. doi: 
      10.1161/01.atv.18.12.1829.