PMID- 16309586
OWN - NLM
STAT- MEDLINE
DCOM- 20070111
LR  - 20161124
IS  - 1165-158X (Electronic)
IS  - 0145-5680 (Linking)
VI  - 51
IP  - 4
DP  - 2005 Sep 30
TI  - Heme oxygenase-1 transduction in endothelial cells causes downregulation of 
      monocyte chemoattractant protein-1 and of genes involved in inflammation and 
      growth.
PG  - 363-70
AB  - Heme oxygenase (HO-1) has been implicated as an anti-inflammatory gene. HO-1 
      overexpression, transiently and chronically, affects heme protein expression, 
      attenuates TNF-mediated cell death, and decreases adhesion molecules. We assessed 
      the effect of oxidant-mediated agents such as glucose and heme on 
      8-epi-isoprostane PGF2alpha (8-epi-PGF2alpha) and monocyte chemoattractant 
      protein-1 (MCP-1). Glucose and heme increased both 8-epi-PGF2alpha and MCP-1. 
      Overexpression of HO-1 decreased both 8-epi-PGF2alpha and MCP-1. To identify 
      target genes involved in HO-1-mediated regulation of inflammation, a serial 
      analysis of gene expression mRNA profile was performed in endothelial cells (EC) 
      overexpressing the human HO-1 gene by transduction of a retrovirus carrying the 
      HO-1 gene. Gene arrays (differential displays among 2400 genes) were used to 
      identify known and novel differentially expressed genes. The levels of expression 
      for several genes were confirmed by real time PCR in cells overexpressing the 
      HO-1 gene. In HO-1 overexpressing cells, VEGF and the prostaglandin transporter 
      were greatly increased while MCP-1 levels were decreased by 2.5-fold. The data 
      from this study are relevant to understanding the mechanisms underlying the 
      pathophysiological effects of HO-1 deficiency on endothelial cell injury and 
      inflammation.
FAU - Sacerdoti, D
AU  - Sacerdoti D
AD  - Department of Clinical and Experimental Medicine, Clinica Medica 5, University of 
      Padova, Via Giustiniani 2, 35100 Padova, Italy. david.sacerdoti@unipd.it
FAU - Colombrita, C
AU  - Colombrita C
FAU - Ghattas, M H
AU  - Ghattas MH
FAU - Ismaeil, E F
AU  - Ismaeil EF
FAU - Scapagnini, G
AU  - Scapagnini G
FAU - Bolognesi, M
AU  - Bolognesi M
FAU - Li Volti, G
AU  - Li Volti G
FAU - Abraham, N G
AU  - Abraham NG
LA  - eng
GR  - HL34300/HL/NHLBI NIH HHS/United States
GR  - HL55601/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20050930
PL  - France
TA  - Cell Mol Biol (Noisy-le-grand)
JT  - Cellular and molecular biology (Noisy-le-Grand, France)
JID - 9216789
RN  - 0 (Chemokine CCL2)
RN  - 42VZT0U6YR (Heme)
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Cell Cycle/*genetics
MH  - Cells, Cultured
MH  - Chemokine CCL2/*metabolism
MH  - *Down-Regulation
MH  - Endothelial Cells/drug effects/enzymology/*metabolism
MH  - Gene Expression Regulation, Enzymologic
MH  - Glucose/pharmacology
MH  - Heme/pharmacology
MH  - Heme Oxygenase-1/*genetics/*metabolism
MH  - Humans
MH  - Inflammation/genetics
MH  - Up-Regulation/genetics
EDAT- 2005/11/29 09:00
MHDA- 2007/01/12 09:00
CRDT- 2005/11/29 09:00
PHST- 2005/05/15 00:00 [received]
PHST- 2005/06/29 00:00 [accepted]
PHST- 2005/11/29 09:00 [pubmed]
PHST- 2007/01/12 09:00 [medline]
PHST- 2005/11/29 09:00 [entrez]
AID - 363 [pii]
PST - epublish
SO  - Cell Mol Biol (Noisy-le-grand). 2005 Sep 30;51(4):363-70.