Compounds > 1-7-bis(4-hydroxy-3-methoxyphenyl)-1-4-6-heptatrien-3-one

1-7-bis(4-hydroxy-3-methoxyphenyl)-1-4-6-heptatrien-3-one and Atherosclerosis

1-7-bis(4-hydroxy-3-methoxyphenyl)-1-4-6-heptatrien-3-one has been researched along with Atherosclerosis* in 1 studies

Other Studies

1 other study(ies) available for 1-7-bis(4-hydroxy-3-methoxyphenyl)-1-4-6-heptatrien-3-one and Atherosclerosis

Article	Year
New therapy via targeting androgen receptor in monocytes/macrophages to battle atherosclerosis. Hypertension (Dallas, Tex. : 1979), 2014, Volume: 63, Issue:6 The male sex has a higher risk to develop coronary artery diseases, including atherosclerosis. The androgen receptor (AR) is expressed in several atherosclerosis-associated cell types, including monocytes/macrophages, endothelial cells (ECs), and smooth muscle cells (SMCs), but its pathophysiological role in each cell type during the development of atherosclerotic lesions remains unclear. Using the Cre-loxP system, we selectively knocked out AR in these 3 cell types and the resultant AR knockout (ARKO) mice, monocyte/macrophage ARKO, EC-ARKO, and SMC-ARKO, were then crossed with the low-density lipoprotein receptor (LDLR) deficient (LDLR(-/-)) mice to develop monocyte/macrophage ARKO-LDLR(-/-), EC-ARKO-LDLR(-/-), and SMC-ARKO-LDLR(-/-) mice for the study of atherosclerosis. The results showed that the monocyte/macrophage ARKO-LDLR(-/-) mice had reduced atherosclerosis compared with the wild-type-LDLR(-/-) control mice. However, no significant difference was detected in EC-ARKO-LDLR(-/-) and SMC-ARKO-LDLR(-/-) mice compared with wild-type-LDLR(-/-) mice, suggesting that the AR in monocytes/macrophages, and not in ECs and SMCs, plays a major role to promote atherosclerosis. Molecular mechanism dissection suggested that AR in monocytes/macrophages upregulated the tumor necrosis factor-α, integrin β2, and lectin-type oxidized LDL receptor 1 molecules that are involved in 3 major inflammation-related processes in atherosclerosis, including monocytes/macrophages migration and adhesion to human umbilical vein ECs, and subsequent foam cell formation. Targeting AR via the AR degradation enhancer, ASC-J9, in wild-type-LDLR(-/-) mice showed similar effects as seen in monocyte/macrophage ARKO-LDLR(-/-) mice with little influence on lipid profile. In conclusion, the AR in monocytes/macrophages plays key roles in atherosclerosis and targeting AR with ASC-J9 may represent a new potential therapeutic approach to battle atherosclerosis. Topics: Animals; Atherosclerosis; Blotting, Western; CD18 Antigens; Cell Adhesion; Cell Line, Tumor; Cell Movement; Cells, Cultured; Curcumin; Diet, High-Fat; Foam Cells; Human Umbilical Vein Endothelial Cells; Humans; Macrophages; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Models, Biological; Monocytes; Myocytes, Smooth Muscle; Receptors, Androgen; Receptors, LDL; Tumor Necrosis Factor-alpha	2014

Article

Year

New therapy via targeting androgen receptor in monocytes/macrophages to battle atherosclerosis.

Hypertension (Dallas, Tex. : 1979), 2014, Volume: 63, Issue:6

The male sex has a higher risk to develop coronary artery diseases, including atherosclerosis. The androgen receptor (AR) is expressed in several atherosclerosis-associated cell types, including monocytes/macrophages, endothelial cells (ECs), and smooth muscle cells (SMCs), but its pathophysiological role in each cell type during the development of atherosclerotic lesions remains unclear. Using the Cre-loxP system, we selectively knocked out AR in these 3 cell types and the resultant AR knockout (ARKO) mice, monocyte/macrophage ARKO, EC-ARKO, and SMC-ARKO, were then crossed with the low-density lipoprotein receptor (LDLR) deficient (LDLR(-/-)) mice to develop monocyte/macrophage ARKO-LDLR(-/-), EC-ARKO-LDLR(-/-), and SMC-ARKO-LDLR(-/-) mice for the study of atherosclerosis. The results showed that the monocyte/macrophage ARKO-LDLR(-/-) mice had reduced atherosclerosis compared with the wild-type-LDLR(-/-) control mice. However, no significant difference was detected in EC-ARKO-LDLR(-/-) and SMC-ARKO-LDLR(-/-) mice compared with wild-type-LDLR(-/-) mice, suggesting that the AR in monocytes/macrophages, and not in ECs and SMCs, plays a major role to promote atherosclerosis. Molecular mechanism dissection suggested that AR in monocytes/macrophages upregulated the tumor necrosis factor-α, integrin β2, and lectin-type oxidized LDL receptor 1 molecules that are involved in 3 major inflammation-related processes in atherosclerosis, including monocytes/macrophages migration and adhesion to human umbilical vein ECs, and subsequent foam cell formation. Targeting AR via the AR degradation enhancer, ASC-J9, in wild-type-LDLR(-/-) mice showed similar effects as seen in monocyte/macrophage ARKO-LDLR(-/-) mice with little influence on lipid profile. In conclusion, the AR in monocytes/macrophages plays key roles in atherosclerosis and targeting AR with ASC-J9 may represent a new potential therapeutic approach to battle atherosclerosis.

Topics: Animals; Atherosclerosis; Blotting, Western; CD18 Antigens; Cell Adhesion; Cell Line, Tumor; Cell Movement; Cells, Cultured; Curcumin; Diet, High-Fat; Foam Cells; Human Umbilical Vein Endothelial Cells; Humans; Macrophages; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Models, Biological; Monocytes; Myocytes, Smooth Muscle; Receptors, Androgen; Receptors, LDL; Tumor Necrosis Factor-alpha

2014