PMID- 15059935
OWN - NLM
STAT- MEDLINE
DCOM- 20041007
LR  - 20220227
IS  - 1524-4571 (Electronic)
IS  - 0009-7330 (Linking)
VI  - 94
IP  - 9
DP  - 2004 May 14
TI  - Critical role of monocyte chemoattractant protein-1 receptor CCR2 on monocytes in 
      hypertension-induced vascular inflammation and remodeling.
PG  - 1203-10
AB  - Activated monocytes are present in the arterial walls of hypertensive patients 
      and animals. Monocyte chemoattractant protein-1 (MCP-1), which controls monocyte 
      function through its receptor (CCR2), is implicated in hypertensive inflammatory 
      changes in the arterial wall. The role of CCR2 expression on monocytes in 
      hypertension-induced vascular remodeling, however, has not been addressed. We 
      hypothesized that CCR2 on monocytes is critical in hypertension-induced vascular 
      inflammation and remodeling. Hypertension was induced by infusion of angiotensin 
      II (Ang II) into wild-type mice, CCR2-deficient (CCR2-/-) mice, and bone 
      marrow-transferred mice with a leukocyte-selective CCR2 deficiency (BMT-CCR2-/-). 
      In wild-type mice, Ang II increased CCR2 intensity in circulating monocytes, 
      which was prevented by an Ang II type-1 (AT1) receptor blocker or blunted in AT1 
      receptor-deficient mice. Enhanced CCR2 intensity on monocytes was observed in 
      hypertensive patients and rats, and was reduced by treatment with the Ang II 
      receptor blocker, supporting the clinical relevance of the observation in mice. 
      In CCR2-/- and BMT-CCR2-/- mice, Ang II-induced vascular inflammation and 
      vascular remodeling (aortic wall thickening and fibrosis) were blunted as 
      compared with control mice. In contrast, Ang II-induced left ventricular 
      hypertrophy developed in CCR2-/- and BMT-CCR2-/- mice. The present study suggests 
      that CCR2 expression in monocytes has a critical role in vascular inflammation 
      and remodeling in Ang II-induced hypertension, and possibly in other forms of 
      hypertension.
FAU - Ishibashi, Minako
AU  - Ishibashi M
AD  - Department of Cardiovascular Medicine, Graduate School of Medical Science, Kyushu 
      University, Fukuoka, Japan.
FAU - Hiasa, Ken-ichi
AU  - Hiasa K
FAU - Zhao, Qingwei
AU  - Zhao Q
FAU - Inoue, Shujiro
AU  - Inoue S
FAU - Ohtani, Kisho
AU  - Ohtani K
FAU - Kitamoto, Shiro
AU  - Kitamoto S
FAU - Tsuchihashi, Miyuki
AU  - Tsuchihashi M
FAU - Sugaya, Takeshi
AU  - Sugaya T
FAU - Charo, Israel F
AU  - Charo IF
FAU - Kura, Shinobu
AU  - Kura S
FAU - Tsuzuki, Teruhisa
AU  - Tsuzuki T
FAU - Ishibashi, Tatsuro
AU  - Ishibashi T
FAU - Takeshita, Akira
AU  - Takeshita A
FAU - Egashira, Kensuke
AU  - Egashira K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20040401
PL  - United States
TA  - Circ Res
JT  - Circulation research
JID - 0047103
RN  - 0 (Angiotensin II Type 1 Receptor Blockers)
RN  - 0 (CCR2 protein, human)
RN  - 0 (Ccr2 protein, mouse)
RN  - 0 (Ccr2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Imidazoles)
RN  - 0 (Receptor, Angiotensin, Type 1)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (Tetrazoles)
RN  - 11128-99-7 (Angiotensin II)
RN  - 6M97XTV3HD (Olmesartan Medoxomil)
RN  - EC 1.14.13.39 (NOS3 protein, human)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 1.14.13.39 (Nos3 protein, mouse)
RN  - EC 1.14.13.39 (Nos3 protein, rat)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - V55S2QJN2X (NG-Nitroarginine Methyl Ester)
SB  - IM
MH  - Angiotensin II/toxicity
MH  - Angiotensin II Type 1 Receptor Blockers
MH  - Animals
MH  - Aorta/drug effects/metabolism
MH  - Bone Marrow Transplantation
MH  - Chemokine CCL2/biosynthesis/genetics
MH  - Chemotaxis, Leukocyte/physiology
MH  - Enzyme Inhibitors/pharmacology
MH  - Humans
MH  - Hypertension/chemically induced/*metabolism
MH  - Hypertrophy, Left Ventricular/etiology/metabolism
MH  - Imidazoles/pharmacology
MH  - Inflammation/metabolism
MH  - Infusion Pumps, Implantable
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Monocytes/drug effects/*physiology
MH  - NG-Nitroarginine Methyl Ester/pharmacology
MH  - Nitric Oxide Synthase/antagonists & inhibitors
MH  - Nitric Oxide Synthase Type II
MH  - Nitric Oxide Synthase Type III
MH  - Olmesartan Medoxomil
MH  - Pilot Projects
MH  - Radiation Chimera
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Receptor, Angiotensin, Type 1/deficiency/genetics
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/deficiency/genetics/*physiology
MH  - Recombinant Fusion Proteins/physiology
MH  - Superoxide Dismutase/genetics
MH  - Tetrazoles/pharmacology
MH  - Up-Regulation/drug effects
EDAT- 2004/04/03 05:00
MHDA- 2004/10/08 09:00
CRDT- 2004/04/03 05:00
PHST- 2004/04/03 05:00 [pubmed]
PHST- 2004/10/08 09:00 [medline]
PHST- 2004/04/03 05:00 [entrez]
AID - 01.RES.0000126924.23467.A3 [pii]
AID - 10.1161/01.RES.0000126924.23467.A3 [doi]
PST - ppublish
SO  - Circ Res. 2004 May 14;94(9):1203-10. doi: 10.1161/01.RES.0000126924.23467.A3. 
      Epub 2004 Apr 1.