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Homocysteine stimulates chemokine expression in the kidney via NF‐kappa B activation
Author(s) -
Hwang SunYoung,
Siow Yaw L.,
Karmin O.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1016.3
Subject(s) - hyperhomocysteinemia , homocysteine , chemokine , kidney , monocyte , medicine , endocrinology , kidney disease , inflammation , immunology
Hyperhomocysteinemia, a condition of elevated blood homocysteine levels, is a risk factor for cardiovascular disorders. Renal disease is an important factor causing hyperhomocysteinemia, the direct effect of homocysteine on the kidney is not well documented. One of the important features in kidney diseases is the infiltration of monocyte/macrophage in the kidney. Monocyte chemoattractant protein‐1 (MCP‐1) is a potent chemokine that stimulates monocyte migration into the tissue. The aim of this study was to investigate the effect of hyperhomocysteinemia on MCP‐1 expression and the underling mechanisms in rat kidneys. Hyperhomocysteinemia was induced in rats fed a high‐methionine diet. The nuclear factor kappa‐B (NF‐κB) activity, the levels of MCP‐1 mRNA and protein were significantly increased in the kidneys of hyperhomocysteinemic rats. Pretreatment of hyperhomocysteinemic rats with a NF‐κB inhibitor completely abolished hyperhomocysteinemia‐induced MCP‐1 expression in the kidney. This further confirmed the causative role of NF‐κB activation in hyperhomocysteinemia‐induced MCP‐1 expression. Taken together, these results suggest that diet‐induced hyperhomocysteinemia can stimulate chemokine expression in the kidney via NF‐κB activation. Such an inflammatory response may contribute to renal injury and chronic systemic inflammation associated with hyperhomocysteinemia.