PMID- 15780578
OWN - NLM
STAT- MEDLINE
DCOM- 20050613
LR  - 20091119
IS  - 0928-8244 (Print)
IS  - 0928-8244 (Linking)
VI  - 44
IP  - 1
DP  - 2005 Apr 1
TI  - Mechanisms of Porphyromonas gingivalis-induced monocyte chemoattractant protein-1 
      expression in endothelial cells.
PG  - 51-8
AB  - Monocyte chemoattractant protein-1 (MCP-1) is expressed in vascular endothelial 
      cells of inflamed gingival tissues and plays an important role in periodontal 
      pathogenesis. Endothelial cells produce high levels of MCP-1 in response to 
      Porphyromonas gingivalis, an important periodontal pathogen. The present study 
      investigated the mechanisms involved in MCP-1 production by human umbilical vein 
      endothelial cells (HUVEC) following infection with P. gingivalis. In contrast to 
      P. gingivalis, Bacteroides forsythus only weakly stimulated MCP-1 production 
      while Treponema denticola could not induce MCP-1 in HUVEC. The MCP-1 production 
      was independent of endogenous interleukin (IL)-1alpha as IL-1 receptor antagonist 
      treatment did not reduce MCP-1 production by P. gingivalis. Meanwhile, 
      antioxidant treatment and inhibition of NAD(P)H oxidase significantly reduced 
      MCP-1 production. Pharmacological inhibition of p38 mitogen-associated protein 
      (MAP) kinase, c-Jun N-terminal kinase (JNK), nuclear factor-kappaB (NF-kappaB) or 
      activator protein-1 (AP-1) also substantially attenuated P. gingivalis-induced 
      MCP-1 expression by HUVEC. Indeed, activation of NF-kappaB and AP-1 was observed 
      in P. gingivalis-infected HUVEC. These results suggest that MCP-1 expression is 
      upregulated in P. gingivalis-infected endothelial cells via reactive oxygen 
      species, p38 MAP kinase, JNK, NF-kappaB, and AP-1.
FAU - Choi, Eun-Kyoung
AU  - Choi EK
AD  - Department of Oral Microbiology, Chonnam National University Dental School, 300 
      Yongbong-Dong, Puk-Gu, Kwangju 500-757, South Korea.
FAU - Park, Sun-Ah
AU  - Park SA
FAU - Oh, Won-Mann
AU  - Oh WM
FAU - Kang, Ho-Cheol
AU  - Kang HC
FAU - Kuramitsu, Howard K
AU  - Kuramitsu HK
FAU - Kim, Byung-Gook
AU  - Kim BG
FAU - Kang, In-Chol
AU  - Kang IC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - FEMS Immunol Med Microbiol
JT  - FEMS immunology and medical microbiology
JID - 9315554
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Transcription Factor AP-1)
RN  - 9007-49-2 (DNA)
RN  - EC 1.6.- (NADH, NADPH Oxidoreductases)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Bacteroidaceae Infections/etiology
MH  - Bacteroides/pathogenicity
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - DNA/genetics
MH  - Endothelium, Vascular/microbiology
MH  - Gene Expression
MH  - Humans
MH  - JNK Mitogen-Activated Protein Kinases/metabolism
MH  - NADH, NADPH Oxidoreductases/metabolism
MH  - NF-kappa B/metabolism
MH  - Periodontitis/etiology
MH  - Porphyromonas gingivalis/*pathogenicity
MH  - RNA, Messenger/genetics/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Transcription Factor AP-1/metabolism
MH  - Treponema denticola/pathogenicity
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
EDAT- 2005/03/23 09:00
MHDA- 2005/06/14 09:00
CRDT- 2005/03/23 09:00
PHST- 2004/08/11 00:00 [received]
PHST- 2004/11/02 00:00 [revised]
PHST- 2004/12/01 00:00 [accepted]
PHST- 2005/03/23 09:00 [pubmed]
PHST- 2005/06/14 09:00 [medline]
PHST- 2005/03/23 09:00 [entrez]
AID - S0928-8244(04)00261-5 [pii]
AID - 10.1016/j.femsim.2004.12.003 [doi]
PST - ppublish
SO  - FEMS Immunol Med Microbiol. 2005 Apr 1;44(1):51-8. doi: 
      10.1016/j.femsim.2004.12.003.