9-deoxy-delta-9-prostaglandin-d2 and Arteriosclerosis

9-deoxy-delta-9-prostaglandin-d2 has been researched along with Arteriosclerosis* in 2 studies

Reviews

1 review(s) available for 9-deoxy-delta-9-prostaglandin-d2 and Arteriosclerosis

ArticleYear
PPAR gamma: an essential role in metabolic control.
    Nutrition, metabolism, and cardiovascular diseases : NMCD, 2001, Volume: 11, Issue:1

    The peroxisome proliferator-activated receptor gamma is a nuclear hormone receptor playing a crucial role in adipogenesis and insulin sensitization. Prostaglandin J2 derivatives and the antidiabetic thiazolidinediones are its respective natural and synthetic ligands. The RXR/PPAR gamma heterodimer has also been reported to have important immunomodulatory activities and its pleiotropic functions suggest wide-ranging medical implications.

    Topics: Adipose Tissue; Animals; Arteriosclerosis; Gene Expression; Humans; Inflammation; Insulin; Ligands; Prostaglandin D2; Receptors, Cytoplasmic and Nuclear; Thiazoles; Thiazolidinediones; Transcription Factors

2001

Other Studies

1 other study(ies) available for 9-deoxy-delta-9-prostaglandin-d2 and Arteriosclerosis

ArticleYear
Macrophages in human atheroma contain PPARgamma: differentiation-dependent peroxisomal proliferator-activated receptor gamma(PPARgamma) expression and reduction of MMP-9 activity through PPARgamma activation in mononuclear phagocytes in vitro.
    The American journal of pathology, 1998, Volume: 153, Issue:1

    Mononuclear phagocytes play an important role in atherosclerosis and its sequela plaque rupture in part by their secretion of matrix metalloproteinases (MMPs), including MMP-9. Peroxisomal proliferator-activated receptor gamma (PPARgamma), a transcription factor in the nuclear receptor superfamily, regulates gene expression in response to various activators, including 15-deoxy-delta12,14-prostaglandin J2 and the antidiabetic agent troglitazone. The role of PPARgamma in human atherosclerosis is unexplored. We report here that monocytes/macrophages in human atherosclerotic lesions (n = 12) express immunostainable PPARgamma. Normal artery specimens (n = 6) reveal minimal immunoreactive PPARgamma. Human monocytes and monocyte-derived macrophages cultured for 6 days in 5% human serum expressed PPARgamma mRNA and protein by reverse transcription-polymerase chain reaction and Western blotting, respectively. In addition, PPARgamma mRNA expression in U937 cells increased during phorbol 12-myristate 13 acetate-induced differentiation. Stimulation of PPARgamma with troglitazone or 15-deoxy-delta12,14-prostaglandin J2 in human monocyte-derived macrophages inhibited MMP-9 gelatinolytic activity in a concentration-dependent fashion as revealed by zymography. This inhibition correlates with decreased MMP-9 secretion as determined by Western blotting. Thus, PPARgamma is present in macrophages in human atherosclerotic lesions and may regulate expression and activity of MMP-9, an enzyme implicated in plaque rupture. PPARgamma is likely to be an important regulator of monocyte/macrophage function with relevance for human atherosclerotic disease.

    Topics: Arteriosclerosis; Blotting, Northern; Blotting, Western; Cell Line; Cells, Cultured; Chromans; Collagenases; Humans; Immunoenzyme Techniques; Macrophages; Matrix Metalloproteinase 9; Monocytes; Prostaglandin D2; Receptors, Cytoplasmic and Nuclear; RNA, Messenger; Tetradecanoylphorbol Acetate; Thiazoles; Thiazolidinediones; Transcription Factors; Troglitazone

1998