PMID- 16794480
OWN - NLM
STAT- MEDLINE
DCOM- 20061019
LR  - 20071115
IS  - 0263-6352 (Print)
IS  - 0263-6352 (Linking)
VI  - 24
IP  - 7
DP  - 2006 Jul
TI  - Deregulated expression of monocyte chemoattractant protein-1 (MCP-1) in arterial 
      hypertension: role in endothelial inflammation and atheromasia.
PG  - 1307-18
AB  - OBJECTIVE: Arterial hypertension is recurrently associated with inflammation of 
      the endothelium as an effect of the upregulation of functional molecules, 
      including cytokines, adhesion molecules and chemokines. However, the role of 
      monocyte chemoattractant protein-1 (MCP-1) in maintaining the inflammatory state 
      of endothelial cells (EC) that leads to the progressive cardiovascular damage is 
      unclear. DESIGN: Here, we investigated the expression of MCP-1, its major cell 
      source as well as recurrence of a defined polymorphism (-2518 MCP-1) apparently 
      linked to endothelial damage in several diseases. METHODS: Serum MCP-1 was 
      measured by enzyme-linked immunosorbent assay (ELISA) in 740 hypertensive 
      patients, subdivided according to their individual organ damage. Expression of 
      both MCP-1 and its receptor CCR2 was evaluated in circulating ECs and macrophages 
      by flow cytometry and real-time reverse transcriptase-polymerase chain reaction 
      (RT-PCR), while gene variants of MCP-1 were revealed by PCR. RESULTS: Soluble 
      MCP-1 was significantly elevated in patients with diffuse atheromasia. 
      Furthermore, it was overexpressed by ECs activated to attract macrophages via the 
      MCP-1/CCR2 pathway, whereas the -2518 MCP-1 polymorphism was correlated with 
      atherosclerosis in most patients. CONCLUSIONS.: Overexpression of MCP-1 is 
      predominant in hypertensive patients with atheromasia in the form of a defined 
      polymorphism. Measurement of MCP-1 may thus reflect the degree of endothelial 
      damage, while early detection of such a polymorphism may acquire a prognostic 
      value in the development of atherosclerosis.
FAU - Tucci, Marco
AU  - Tucci M
AD  - DIMO, Department of Internal Medicine and Clinical Oncology, University of Bari, 
      Italy. m.tucci@dimo.uniba.it
FAU - Quatraro, Cosima
AU  - Quatraro C
FAU - Frassanito, Maria Antonia
AU  - Frassanito MA
FAU - Silvestris, Franco
AU  - Silvestris F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - J Hypertens
JT  - Journal of hypertension
JID - 8306882
RN  - 0 (CCL2 protein, human)
RN  - 0 (CCR2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
RN  - EC 3.4.- (Metalloproteases)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Atherosclerosis/blood
MH  - Chemokine CCL2/*blood/genetics
MH  - Endothelium, Vascular/*metabolism/pathology
MH  - Female
MH  - Genotype
MH  - Humans
MH  - Hypertension/*blood/physiopathology
MH  - Macrophages/*metabolism
MH  - Male
MH  - Metalloproteases/metabolism
MH  - Middle Aged
MH  - Odds Ratio
MH  - Polymorphism, Genetic/*genetics/physiology
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/metabolism
MH  - Statistics, Nonparametric
MH  - Vasculitis/*blood
EDAT- 2006/06/24 09:00
MHDA- 2006/10/20 09:00
CRDT- 2006/06/24 09:00
PHST- 2006/06/24 09:00 [pubmed]
PHST- 2006/10/20 09:00 [medline]
PHST- 2006/06/24 09:00 [entrez]
AID - 00004872-200607000-00016 [pii]
AID - 10.1097/01.hjh.0000234111.31239.c3 [doi]
PST - ppublish
SO  - J Hypertens. 2006 Jul;24(7):1307-18. doi: 10.1097/01.hjh.0000234111.31239.c3.