PMID- 18164016
OWN - NLM
STAT- MEDLINE
DCOM- 20080623
LR  - 20211125
IS  - 1879-1484 (Electronic)
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 198
IP  - 2
DP  - 2008 Jun
TI  - Glycated LDL increases monocyte CC chemokine receptor 2 expression and monocyte 
      chemoattractant protein-1-mediated chemotaxis.
PG  - 307-12
LID - 10.1016/j.atherosclerosis.2007.10.035 [doi]
AB  - BACKGROUND: Previous reports have suggested that levels of advanced glycation end 
      product-modified LDL (AGE-LDL) increase in patients with diabetes due to elevated 
      plasma glucose. However, understanding of the mechanisms by which AGE-LDL may 
      accelerate atherogenesis remains incomplete. METHODS AND RESULTS: Microarray and 
      reverse transcription real-time PCR (RT-PCR) analyses revealed that AGE-LDL 
      significantly increased levels of CC chemokine receptor 2 (CCR2) mRNA in human 
      macrophages compared with LDL, an effect accompanied by increased levels of CCR2 
      protein. Flow cytometry also showed that AGE-LDL increases CCR2 expression on the 
      cell surface following stimulation (48h) (P<0.05). This effect appeared to depend 
      on the receptor for AGE (RAGE), since an anti-RAGE antibody significantly blocked 
      increased CCR2 mRNA. Functional studies demonstrated that exposure of THP-1 
      monocytoid cells to AGE-LDL increases chemotaxis mediated by monocyte 
      chemoattractant protein-1 (MCP-1) up to 3-fold compared to LDL treatment 
      (P<0.05). CONCLUSIONS: These data show that AGE-LDL can increase CCR2 expression 
      in macrophages and stimulate the chemotactic response elicited by MCP-1. This 
      novel mechanism may contribute to accelerated atherogenesis in diabetic patients.
FAU - Isoda, Kikuo
AU  - Isoda K
AD  - Donald W. Reynolds Cardiovascular Clinical Research Center, Brigham and Women's 
      Hospital, Harvard Medical School, Boston, MA 02115, USA.
FAU - Folco, Eduardo
AU  - Folco E
FAU - Marwali, M Reza
AU  - Marwali MR
FAU - Ohsuzu, Fumitaka
AU  - Ohsuzu F
FAU - Libby, Peter
AU  - Libby P
LA  - eng
GR  - R01 HL034636/HL/NHLBI NIH HHS/United States
GR  - R01 HL034636-20/HL/NHLBI NIH HHS/United States
GR  - R37 HL034636/HL/NHLBI NIH HHS/United States
GR  - HL-34636/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 - 20071227
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Chemokine CCL2)
RN  - 0 (Glycation End Products, Advanced)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, CCR2)
RN  - 0 (glycated lipoproteins, LDL)
SB  - IM
MH  - Cell Membrane/metabolism
MH  - Cells, Cultured
MH  - Chemokine CCL2/pharmacology
MH  - *Chemotaxis/drug effects
MH  - Glycation End Products, Advanced/*metabolism/pharmacology
MH  - Humans
MH  - Lipoproteins, LDL/*metabolism/pharmacology
MH  - Macrophages/drug effects/*immunology
MH  - Monocytes/drug effects/immunology
MH  - RNA, Messenger/metabolism
MH  - Receptors, CCR2/genetics/*metabolism
PMC - PMC2453313
MID - NIHMS54562
EDAT- 2008/01/01 09:00
MHDA- 2008/06/24 09:00
PMCR- 2009/06/01
CRDT- 2008/01/01 09:00
PHST- 2006/09/26 00:00 [received]
PHST- 2007/09/12 00:00 [revised]
PHST- 2007/10/22 00:00 [accepted]
PHST- 2008/01/01 09:00 [pubmed]
PHST- 2008/06/24 09:00 [medline]
PHST- 2008/01/01 09:00 [entrez]
PHST- 2009/06/01 00:00 [pmc-release]
AID - S0021-9150(07)00667-3 [pii]
AID - 10.1016/j.atherosclerosis.2007.10.035 [doi]
PST - ppublish
SO  - Atherosclerosis. 2008 Jun;198(2):307-12. doi: 
      10.1016/j.atherosclerosis.2007.10.035. Epub 2007 Dec 27.