RGD Reference Report - Folic acid treatment reduces chemokine release from peripheral blood mononuclear cells in hyperhomocysteinemic subjects. - Rat Genome Database

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Folic acid treatment reduces chemokine release from peripheral blood mononuclear cells in hyperhomocysteinemic subjects.

Authors: Holven, KB  Aukrust, P  Holm, T  Ose, L  Nenseter, MS 
Citation: Holven KB, etal., Arterioscler Thromb Vasc Biol. 2002 Apr 1;22(4):699-703.
RGD ID: 5135249
Pubmed: PMID:11950713   (View Abstract at PubMed)

Elevated plasma homocysteine concentration is an independent risk factor for cardiovascular disease. However, the mechanisms by which hyperhomocysteinemia induces vascular disease are uncertain. An early step in atherogenesis involves leukocyte migration into the arterial wall, a process regulated in part by chemokines. We hypothesized that homocysteine may exert its atherogenic effect in part through chemokine-mediated mechanisms, and in the present study, we examined the effects of folic acid supplementation for 6 weeks on chemokine levels in hyperhomocysteinemic individuals. Data showed the following: (1) Compared with control subjects, hyperhomocysteinemic subjects had elevated plasma levels of the CXC chemokines, epithelial neutrophil-activating peptide (ENA)-78 (P<0.05), and growth-regulated oncogene (GRO)alpha (P=0.088), and homocysteine was significantly correlated with ENA-78 and GROalpha. (2) During folic acid treatment, normalization of homocysteine levels was accompanied by a marked reduction in oxidized low density lipoprotein-stimulated release of CXC chemokines (ie, GROalpha, ENA-78, and interleukin-8) and CC chemokines (ie, monocyte chemoattractant peptide-1 and RANTES) in peripheral blood mononuclear cells from these individuals. (3) The oxidized low density lipoprotein-induced release of ENA-78 from peripheral blood mononuclear cells from control subjects was significantly reduced when cells were incubated in the presence of folic acid. These data may suggest that homocysteine exerts atherogenic effects in part by enhancing chemokine responses in cells involved in atherogenesis and that folic acid supplementation may downregulate these inflammatory responses.




  
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
CXCL1Humanhyperhomocysteinemia  IEP protein:increased expression:plasmaRGD 
CXCL5Humanhyperhomocysteinemia  IEP protein:increased expression:plasmaRGD 
Cxcl1Rathyperhomocysteinemia  ISOCXCL1 (Homo sapiens)protein:increased expression:plasmaRGD 
Cxcl1Mousehyperhomocysteinemia  ISOCXCL1 (Homo sapiens)protein:increased expression:plasmaRGD 
Cxcl5Mousehyperhomocysteinemia  ISOCXCL6 (Homo sapiens)protein:increased expression:plasmaRGD 
Cxcl6Rathyperhomocysteinemia  ISOCXCL6 (Homo sapiens)protein:increased expression:plasmaRGD 


Genes (Rattus norvegicus)
Cxcl1  (C-X-C motif chemokine ligand 1) Cxcl6  (C-X-C motif chemokine ligand 6)

Genes (Mus musculus)
Cxcl1  (C-X-C motif chemokine ligand 1) Cxcl5  (C-X-C motif chemokine ligand 5)

Genes (Homo sapiens)
CXCL1  (C-X-C motif chemokine ligand 1) CXCL5  (C-X-C motif chemokine ligand 5)