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Thiazolidinedione inhibits the production of monocyte chemoattractant protein‐1 in cytokine‐treated human vascular endothelial cells
Author(s) -
Murao Koji,
Imachi Hitomi,
Momoi Atsuko,
Sayo Yoshitaka,
Hosokawa Hitoshi,
Sato Makoto,
Ishida Toshihiko,
Takahara Jiro
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00765-6
Subject(s) - monocyte , thiazolidinedione , chemokine , chemotaxis , ccl2 , tumor necrosis factor alpha , cytokine , medicine , chemistry , microbiology and biotechnology , endocrinology , cancer research , biology , inflammation , receptor , type 2 diabetes , diabetes mellitus
The chemokine monocyte chemoattractant protein‐1 is a potent chemoattractant for monocytes. Monocyte chemoattractant protein‐1 is produced by vascular endothelial cells during inflammatory diseases such as atherosclerosis. In this study, we examined the effects of a thiazolidinedione on monocyte chemoattractant protein‐1 expression in human vascular endothelial cells. In human vascular endothelial cells, interleukin‐1β and tumor necrosis factor‐α induced endogenous monocyte chemoattractant protein‐1 protein secretion, mRNA expression and promoter activity. The thiazolidinedione inhibited these effects. In summary, our results indicated that the suppression of the expression of monocyte chemoattractant protein‐1 can be accomplished by thiazolidinedione treatment, raising the possibility that thiazolidinedione may be of therapeutic value in the treatment of diseases such as atherosclerosis.