PMID- 20467793
OWN - NLM
STAT- MEDLINE
DCOM- 20110104
LR  - 20211020
IS  - 1573-4919 (Electronic)
IS  - 0300-8177 (Linking)
VI  - 342
IP  - 1-2
DP  - 2010 Sep
TI  - The effects of ox-LDL in human atherosclerosis may be mediated in part via the 
      toll-like receptor 4 pathway.
PG  - 201-6
LID - 10.1007/s11010-010-0484-8 [doi]
AB  - Toll-like receptor 4 (TLR4) may provide a potential pathophysiological link 
      between lipids and infection/inflammation and atherosclerosis. Oxidized 
      low-density lipoprotein (ox-LDL) makes it more atherogenic than its native form. 
      The purpose of the study was to investigate the relationship between the effects 
      of ox-LDL in human atherosclerosis and the expression of TLR4. We studied the 
      relationship between TLR4 and ox-LDL, pro and con, using both real-time 
      quantitative RT-PCR and RNA interference technology through in vitro cell 
      culture. Nuclear factor kappa B (NF-kappa B) activity and the concentrations of 
      monocyte chemoattractant protein-1(MCP-1) and interleukin-8 (IL-8) were detected 
      by ELISA. The results showed that the expression of TLR4 increased in response to 
      ox-LDL. Simultaneously, NF-kappa B relative activity and the concentrations of 
      MCP-1 and IL-8 in cell supernatant were upregulated by ox-LDL in a dose-dependent 
      manner. TLR4 expression was inhibited by small interference RNA(siRNA) plasmid 
      expression vectors; NF-kappa B activity and the secretions of MCP-1 and IL-8 in 
      response to ox-LDL were significantly lower in the group wherein TLR4 expression 
      has been inhibited than that in the group wherein TLR4 expression has not been 
      inhibited. We suggest that the atherogenic effects of ox-LDL could be mediated in 
      part via the TLR4 pathway. Furthermore, inhibition of TLR4 expression may 
      downregulate the NF-kappa B activity and secretions of MCP-1 and IL-8 in 
      monocytes due to oxidized LDL, resulting in the alleviation of the progress of 
      atherosclerosis.
FAU - Geng, Honglian
AU  - Geng H
AD  - Department of Laboratory Diagnosis, Changzheng Hospital, Second Military Medical 
      University, Shanghai, China. hlgeng@yahoo.com.cn
FAU - Wang, Aihua
AU  - Wang A
FAU - Rong, Guanghua
AU  - Rong G
FAU - Zhu, Bei
AU  - Zhu B
FAU - Deng, Yan
AU  - Deng Y
FAU - Chen, Jun
AU  - Chen J
FAU - Zhong, Renqian
AU  - Zhong R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100514
PL  - Netherlands
TA  - Mol Cell Biochem
JT  - Molecular and cellular biochemistry
JID - 0364456
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (TLR4 protein, human)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (oxidized low density lipoprotein)
SB  - IM
MH  - Atherosclerosis/*metabolism/pathology
MH  - Blotting, Western
MH  - Chemokine CCL2/genetics/metabolism
MH  - Humans
MH  - Interleukin-8/genetics/metabolism
MH  - Lipoproteins, LDL/*pharmacology
MH  - NF-kappa B/genetics/metabolism
MH  - Oxidation-Reduction
MH  - RNA, Messenger/genetics
MH  - RNA, Small Interfering/pharmacology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/*drug effects
MH  - Toll-Like Receptor 4/antagonists & inhibitors/genetics/*metabolism
MH  - U937 Cells
EDAT- 2010/05/15 06:00
MHDA- 2011/01/05 06:00
CRDT- 2010/05/15 06:00
PHST- 2010/01/11 00:00 [received]
PHST- 2010/05/04 00:00 [accepted]
PHST- 2010/05/15 06:00 [entrez]
PHST- 2010/05/15 06:00 [pubmed]
PHST- 2011/01/05 06:00 [medline]
AID - 10.1007/s11010-010-0484-8 [doi]
PST - ppublish
SO  - Mol Cell Biochem. 2010 Sep;342(1-2):201-6. doi: 10.1007/s11010-010-0484-8. Epub 
      2010 May 14.