PMID- 15689417
OWN - NLM
STAT- MEDLINE
DCOM- 20050801
LR  - 20161124
IS  - 1096-6080 (Print)
IS  - 1096-0929 (Linking)
VI  - 85
IP  - 1
DP  - 2005 May
TI  - Oxidative stress mediates sodium arsenite-induced expression of heme oxygenase-1, 
      monocyte chemoattractant protein-1, and interleukin-6 in vascular smooth muscle 
      cells.
PG  - 541-50
AB  - Arsenic exposure is associated with an increased risk of vascular disorders, and 
      results in increased oxidative stress in endothelial cells and vascular smooth 
      muscle cells (VSMCs). Since oxidative stress is involved in regulating the 
      expression of genes related to atherogenesis, we investigated its involvement in 
      the enhanced expression of three atherosclerosis-related genes coding for heme 
      oxygenase-1 (HO-1), monocyte chemoattractant protein-1 (MCP-1), and interleukin-6 
      (IL-6) in VSMCs treated with inorganic sodium arsenite (iAs). In human VSMCs 
      (hVSMCs) and rat VSMCs (rVSMCs), HO-1, MCP-1, and IL-6 mRNA levels were 
      significantly increased by iAs treatment. An increase in HO-1 protein levels in 
      hVSMCs was confirmed by Western blotting technique, while increased MCP-1 and 
      IL-6 secretion by hVSMCs was demonstrated by enzyme-linked immunosorbent assay. 
      Although modulators of oxidative stress inhibited this iAs-induced increase in 
      the expression of these three genes, different modulators had differential 
      effects. In iAs-treated rVSMCs, catalase, dimethylsulfoxide, and 
      L-omega-nitro-L-arginine significantly inhibited the increase in expression of 
      all three genes, allopurinol inhibited the increase in MCP-1 and IL-6 expression, 
      but had no effect on HO-1 expression, while superoxide dismutase had no 
      significant effect on HO-1 expression, but had an inhibitory effect on IL-6 
      expression and a stimulatory effect on MCP-1 expression. Therefore, iAs may 
      enhance the expression of HO-1, MCP-1, and IL-6 in VSMCs via different reactive 
      oxygen molecules. Furthermore, using tin protoporphyrin IX (SnPP) and anti-MCP-1 
      antibody to abolish iAs-induced HO-1 and MCP-1 activity, respectively, shows that 
      HO-1 has protective effect against iAs-induced injury in VSMCs and MCP-1 is 
      chemoattractive to human monocytes, THP-1.
FAU - Lee, Pei-Chung
AU  - Lee PC
AD  - Institute of Biopharmaceutical Science, School of Life Sciences, National 
      Yang-Ming University, Pei-Tou, Taipei, Taiwan, ROC.
FAU - Ho, I-Ching
AU  - Ho IC
FAU - Lee, Te-Chang
AU  - Lee TC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20050202
PL  - United States
TA  - Toxicol Sci
JT  - Toxicological sciences : an official journal of the Society of Toxicology
JID - 9805461
RN  - 0 (Arsenites)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Membrane Proteins)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Sodium Compounds)
RN  - 48OVY2OC72 (sodium arsenite)
RN  - EC 1.14.14.18 (HMOX1 protein, human)
RN  - EC 1.14.14.18 (Heme Oxygenase (Decyclizing))
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
SB  - IM
MH  - Animals
MH  - Aorta
MH  - Arsenites/*toxicity
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics
MH  - Chemotaxis, Leukocyte/drug effects
MH  - Fibroblasts/drug effects/metabolism
MH  - Gene Expression/*drug effects
MH  - Heme Oxygenase (Decyclizing)/genetics
MH  - Heme Oxygenase-1
MH  - Humans
MH  - Interleukin-6/genetics
MH  - Membrane Proteins
MH  - Monocytes/drug effects
MH  - *Muscle, Smooth, Vascular/cytology/drug effects/metabolism
MH  - Oxidative Stress/*drug effects
MH  - Rats
MH  - Reactive Oxygen Species/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Sodium Compounds/*toxicity
EDAT- 2005/02/04 09:00
MHDA- 2005/08/02 09:00
CRDT- 2005/02/04 09:00
PHST- 2005/02/04 09:00 [pubmed]
PHST- 2005/08/02 09:00 [medline]
PHST- 2005/02/04 09:00 [entrez]
AID - kfi101 [pii]
AID - 10.1093/toxsci/kfi101 [doi]
PST - ppublish
SO  - Toxicol Sci. 2005 May;85(1):541-50. doi: 10.1093/toxsci/kfi101. Epub 2005 Feb 2.