PMID- 17529908
OWN - NLM
STAT- MEDLINE
DCOM- 20070927
LR  - 20161122
IS  - 1073-2322 (Print)
IS  - 1073-2322 (Linking)
VI  - 28
IP  - 2
DP  - 2007 Aug
TI  - Mechanisms of oxidant regulation of monocyte chemotactic protein 1 production in 
      human whole blood and isolated mononuclear cells.
PG  - 178-85
AB  - Previous work has demonstrated that reactive oxygen intermediates (ROIs) play an 
      important regulatory role in the induction of monocyte chemotactic protein 1 
      (MCP-1) in certain cells. This study investigated the mechanisms of ROI 
      regulation of MCP-1 gene expression in whole blood and isolated peripheral blood 
      mononuclear cells (PBMCs). The antioxidants dimethyl sulfoxide (DMSO), N-acetyl 
      cysteine, and dimethyl thiourea significantly inhibited lipopolysaccharide 
      (LPS)-induced MCP-1 production in either whole blood or isolated blood cells. In 
      contrast, interleukin 6 and tumor necrosis factor production were not affected 
      and interleukin-1beta levels were actually increased with DMSO treatment. 
      Exogenous ROI (either hydrogen peroxide or O2 generated by xanthine/xanthine 
      oxidase) stimulated MCP-1 production, which was also inhibited by DMSO. To 
      confirm the biological relevance of these findings in vivo, mice treated with 
      DMSO before LPS challenge had significantly lower plasma levels of MCP-1. The 
      level of inhibition was addressed in experiments which demonstrated that DMSO 
      significantly decreased MCP-1 mRNA induced by LPS in whole blood and PBMCs. 
      Cycloheximide treatment did not abolish the DMSO inhibition of MCP-1 mRNA, 
      demonstrating that de novo protein synthesis is not required. Treatment with 
      actinomycin D showed that DMSO did not increase the decay rate of MCP-1 mRNA, 
      indicating that ROI did not change the stability of MCP-1 mRNA. These results 
      provide evidence that in whole blood and PBMCs, DMSO regulates MCP-1 gene 
      expression by decreasing the induction of MCP-1 mRNA.
FAU - Xing, Liyu
AU  - Xing L
AD  - Department of Pathology, University of Michigan, Medical School Ann Arbor, Ann 
      Arbor, MI, USA. remickd@bu.edu
FAU - Remick, Daniel G
AU  - Remick DG
LA  - eng
GR  - R01 GM050401/GM/NIGMS NIH HHS/United States
GR  - R01 GM050401-13/GM/NIGMS NIH HHS/United States
GR  - ES 09589/ES/NIEHS NIH HHS/United States
GR  - GM 50403/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Antioxidants)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Oxidants)
SB  - IM
MH  - Animals
MH  - Antioxidants/physiology
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis
MH  - Female
MH  - Humans
MH  - Leukocytes, Mononuclear/*metabolism
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Oxidants/*physiology
EDAT- 2007/05/29 09:00
MHDA- 2007/09/28 09:00
CRDT- 2007/05/29 09:00
PHST- 2007/05/29 09:00 [pubmed]
PHST- 2007/09/28 09:00 [medline]
PHST- 2007/05/29 09:00 [entrez]
AID - 10.1097/shk.0b013e3180311cf4 [doi]
PST - ppublish
SO  - Shock. 2007 Aug;28(2):178-85. doi: 10.1097/shk.0b013e3180311cf4.