PMID- 17466307
OWN - NLM
STAT- MEDLINE
DCOM- 20080229
LR  - 20210108
IS  - 1879-1484 (Electronic)
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 196
IP  - 1
DP  - 2008 Jan
TI  - Toll-like receptor 2 plays a critical role in the progression of atherosclerosis 
      that is independent of dietary lipids.
PG  - 146-154
LID - S0021-9150(07)00188-8 [pii]
LID - 10.1016/j.atherosclerosis.2007.03.025 [doi]
AB  - OBJECTIVE: Toll-like receptors (TLRs), a group of pathogen-associated microbial 
      pattern recognition receptors, play an important role in innate immune signaling 
      and are differentially regulated in chronic inflammatory diseases such as 
      atherosclerosis. However, the involvement of TLRs in the progression of 
      atherosclerosis is still unclear. METHODS AND RESULTS: TLR2 and apolipoprotein E 
      double knockout (Tlr2(-/-)Apoe(-/-)) mice were generated and the progressive 
      formation of atherosclerotic plaque in the aortas was examined in mice fed a 
      normal chow diet. We demonstrate that inactivation of TLR2 resulted in reduced 
      progression of atherosclerosis in both male and female Apoe(-/-) mice. Likewise, 
      TLR2 deficiency resulted in a reduction in lipid accumulation and decreased 
      macrophage recruitment to the aortic sinus, as well as reduced monocyte 
      chemoattractant protein-1 (MCP-1) levels. Furthermore, macrophages isolated from 
      Tlr2(-/-)Apoe(-/-) mice demonstrated significantly reduced MCP-1 production upon 
      stimulation with a TLR2 ligand. However, no differences in acetylated low-density 
      lipoprotein uptake and foam cell formation were observed in macrophages isolated 
      from Tlr2(-/-)Apoe(-/-) mice as compared to Apoe(-/-) mice. CONCLUSIONS: TLR2 
      plays a critical role in the progression of atherosclerosis in Apoe(-/-) mice, 
      which is independent of dietary lipids and macrophage lipid uptake.
FAU - Liu, Xinyan
AU  - Liu X
AD  - Department of Medicine, Section of Molecular Medicine, Boston University School 
      of Medicine, 650 Albany Street, Boston, MA 02118, United States.
FAU - Ukai, Takashi
AU  - Ukai T
AD  - Department of Medicine, Section of Molecular Medicine, Boston University School 
      of Medicine, 650 Albany Street, Boston, MA 02118, United States; Department of 
      Periodontology, Unit of Translational Medicine, Course of Medical and Dental 
      Sciences, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 
      852-8588, Japan.
FAU - Yumoto, Hiromichi
AU  - Yumoto H
AD  - Department of Medicine, Section of Molecular Medicine, Boston University School 
      of Medicine, 650 Albany Street, Boston, MA 02118, United States; Department of 
      Conservative Dentistry, The Institute of Health Biosciences, The University of 
      Tokushima Graduate School, Tokushima 770-8504, Japan.
FAU - Davey, Michael
AU  - Davey M
AD  - Department of Periodontology and Oral Biology, Goldman School of Dental Medicine, 
      Boston University, Boston, MA 02118, United States.
FAU - Goswami, Sulip
AU  - Goswami S
AD  - Department of Medicine, Section of Molecular Medicine, Boston University School 
      of Medicine, 650 Albany Street, Boston, MA 02118, United States.
FAU - Gibson, Frank C 3rd
AU  - Gibson FC 3rd
AD  - Department of Medicine, Section of Molecular Medicine, Boston University School 
      of Medicine, 650 Albany Street, Boston, MA 02118, United States.
FAU - Genco, Caroline A
AU  - Genco CA
AD  - Department of Medicine, Section of Molecular Medicine, Boston University School 
      of Medicine, 650 Albany Street, Boston, MA 02118, United States; Department of 
      Periodontology and Oral Biology, Goldman School of Dental Medicine, Boston 
      University, Boston, MA 02118, United States; Department of Microbiology, Boston 
      University School of Medicine, Boston, MA 02118, United States. Electronic 
      address: caroline.genco@bmc.org.
LA  - eng
GR  - R01 DE014774/DE/NIDCR NIH HHS/United States
GR  - R01 HL080387-02/HL/NHLBI NIH HHS/United States
GR  - DE014774/DE/NIDCR NIH HHS/United States
GR  - HL080387/HL/NHLBI NIH HHS/United States
GR  - R01 HL080387/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20070426
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Apolipoproteins E)
RN  - 0 (Dietary Fats)
RN  - 0 (Toll-Like Receptor 2)
SB  - IM
MH  - Animals
MH  - Aorta/physiopathology
MH  - Apolipoproteins E/genetics
MH  - Atherosclerosis/immunology/*physiopathology
MH  - Dietary Fats/pharmacology
MH  - Disease Models, Animal
MH  - Female
MH  - Foam Cells/*immunology
MH  - Inflammation/metabolism/physiopathology
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Toll-Like Receptor 2/*physiology
PMC - PMC2243224
MID - NIHMS39404
EDAT- 2007/05/01 09:00
MHDA- 2008/03/01 09:00
PMCR- 2009/01/01
CRDT- 2007/05/01 09:00
PHST- 2006/12/18 00:00 [received]
PHST- 2007/03/05 00:00 [revised]
PHST- 2007/03/13 00:00 [accepted]
PHST- 2007/05/01 09:00 [pubmed]
PHST- 2008/03/01 09:00 [medline]
PHST- 2007/05/01 09:00 [entrez]
PHST- 2009/01/01 00:00 [pmc-release]
AID - S0021-9150(07)00188-8 [pii]
AID - 10.1016/j.atherosclerosis.2007.03.025 [doi]
PST - ppublish
SO  - Atherosclerosis. 2008 Jan;196(1):146-154. doi: 
      10.1016/j.atherosclerosis.2007.03.025. Epub 2007 Apr 26.