cay-10404 and Disease-Models--Animal

cay-10404 has been researched along with Disease-Models--Animal* in 1 studies

Other Studies

1 other study(ies) available for cay-10404 and Disease-Models--Animal

Article	Year
High-density lipoproteins suppress chemokines and chemokine receptors in vitro and in vivo. Arteriosclerosis, thrombosis, and vascular biology, 2010, Volume: 30, Issue:9 To investigate whether high-density lipoproteins (HDLs) suppress chemokine (CCL2, CCL5, and CX(3)CL1) and chemokine receptor (CCR2 and CX(3)CR1) expression, a mechanism for the atheroprotective properties of HDLs.. Apolipoprotein (apo) E(-/-) mice were fed a high-fat diet for 12 weeks. Before being euthanized, the mice received 5 consecutive daily injections of lipid-free apoA-I, 40 mg/kg, or saline (control). The injection of apoA-I reduced CCR2 and CX(3)CR1 expression in plaques compared with controls (P<0.05). ApoA-I-injected mice had lower plasma CCL2 and CCL5 levels. Hepatic CCL2, CCL5, and CX(3)CL1 levels were also reduced (P<0.05). In vitro studies found that reconstituted HDL (rHDL) reduced monocyte CCR2 and CX(3)CR1 expression and inhibited their migration toward CCL2 and CX(3)CL1 (P<0.05). Preincubation with rHDL reduced CCL2, CCL5, and CX(3)CL1 expression in monocytes and human coronary artery endothelial cells. The stimulation of CX(3)CR1 with peroxisome proliferator-activated receptor gamma agonist CAY10410 was suppressed by preincubation with rHDL but did not affect the peroxisome proliferator-activated receptor gamma antagonist (GW9664)-mediated increase in CCR2. In monocytes and human coronary artery endothelial cells, rHDL reduced the expression of the nuclear p65 subunit, IkappaB kinase activity, and the phosphorylation of IkappaBalpha (P<0.05).. Lipid-free apoA-I and rHDL reduce the expression of chemokines and chemokine receptors in vivo and in vitro via modulation of nuclear factor kappaB and peroxisome proliferator-activated receptor gamma. Topics: Animals; Apolipoprotein A-I; Apolipoproteins E; Atherosclerosis; Cells, Cultured; Chemokine CCL2; Chemokine CCL5; Chemokine CX3CL1; Chemokines; Chemotaxis, Leukocyte; Disease Models, Animal; Down-Regulation; Endothelial Cells; Humans; I-kappa B Proteins; Injections, Intravenous; Isoxazoles; Lipoproteins, HDL; Mice; Mice, Inbred C57BL; Mice, Knockout; Monocytes; NF-KappaB Inhibitor alpha; Phosphorylation; PPAR gamma; Receptors, CCR2; Receptors, Chemokine; Receptors, Interleukin-8A; RNA, Messenger; Sulfones; Transcription Factor RelA	2010

Article

Year

High-density lipoproteins suppress chemokines and chemokine receptors in vitro and in vivo.

Arteriosclerosis, thrombosis, and vascular biology, 2010, Volume: 30, Issue:9

To investigate whether high-density lipoproteins (HDLs) suppress chemokine (CCL2, CCL5, and CX(3)CL1) and chemokine receptor (CCR2 and CX(3)CR1) expression, a mechanism for the atheroprotective properties of HDLs.. Apolipoprotein (apo) E(-/-) mice were fed a high-fat diet for 12 weeks. Before being euthanized, the mice received 5 consecutive daily injections of lipid-free apoA-I, 40 mg/kg, or saline (control). The injection of apoA-I reduced CCR2 and CX(3)CR1 expression in plaques compared with controls (P<0.05). ApoA-I-injected mice had lower plasma CCL2 and CCL5 levels. Hepatic CCL2, CCL5, and CX(3)CL1 levels were also reduced (P<0.05). In vitro studies found that reconstituted HDL (rHDL) reduced monocyte CCR2 and CX(3)CR1 expression and inhibited their migration toward CCL2 and CX(3)CL1 (P<0.05). Preincubation with rHDL reduced CCL2, CCL5, and CX(3)CL1 expression in monocytes and human coronary artery endothelial cells. The stimulation of CX(3)CR1 with peroxisome proliferator-activated receptor gamma agonist CAY10410 was suppressed by preincubation with rHDL but did not affect the peroxisome proliferator-activated receptor gamma antagonist (GW9664)-mediated increase in CCR2. In monocytes and human coronary artery endothelial cells, rHDL reduced the expression of the nuclear p65 subunit, IkappaB kinase activity, and the phosphorylation of IkappaBalpha (P<0.05).. Lipid-free apoA-I and rHDL reduce the expression of chemokines and chemokine receptors in vivo and in vitro via modulation of nuclear factor kappaB and peroxisome proliferator-activated receptor gamma.

Topics: Animals; Apolipoprotein A-I; Apolipoproteins E; Atherosclerosis; Cells, Cultured; Chemokine CCL2; Chemokine CCL5; Chemokine CX3CL1; Chemokines; Chemotaxis, Leukocyte; Disease Models, Animal; Down-Regulation; Endothelial Cells; Humans; I-kappa B Proteins; Injections, Intravenous; Isoxazoles; Lipoproteins, HDL; Mice; Mice, Inbred C57BL; Mice, Knockout; Monocytes; NF-KappaB Inhibitor alpha; Phosphorylation; PPAR gamma; Receptors, CCR2; Receptors, Chemokine; Receptors, Interleukin-8A; RNA, Messenger; Sulfones; Transcription Factor RelA

2010