18 research outputs found

    TRAF6 expression in blood does not associate with acute or chronic coronary heart disease.

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    <p>325 patients undergoing coronary angiography were divided into three groups: no coronary heart disease (No CHD, N = 77), stable coronary heart disease (CHD, N = 178), and acute coronary syndromes (ACS, N = 70). TRAF6 and GAPDH mRNA was analyzed by quantitative real-time PCR in total blood RNA. Results are presented as mean±SD computed from the average measurements obtained from each group.</p

    TRAF6 deficiency does not modulate inflammatory reactivity of macrophages toward cholesterol and palmitic acid.

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    <p>Bone marrow-derived macrophages were isolated from 6 week old TRAF6<sup>+/+</sup>/LDLR<sup>−/−</sup> mice receiving TRAF6-deficient (hatched bars, N = 4) or competent fetal liver cells (white bars, N = 4), were stimulated with 4 mg/ml cholesterol or 0.75 µM palmitic acid, and assayed for expression of IL-6 (A), MCP-1 (B), TNFα (C), and IL12-p70 (D) by cytometric bead array.</p

    TRAF6 deficiency does not modulate atherogenesis in mice.

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    <p>Lethally irradiated 6 week old TRAF6<sup>+/+</sup>/LDLR<sup>−/−</sup> mice received TRAF6-deficient (hatched bars, N = 21) or competent fetal liver cells (white bars, N = 21), TRAF6<sup>+/−</sup>/LDLR<sup>−/−</sup> mice received TRAF6-deficient fetal liver cells (black bars, N = 22) only. Subsequently, all groups consumed high cholesterol diet (HCD) for 18 weeks. Intimal lesion area of the atherosclerotic plaques in aortic roots was quantified. Pooled mean intimal lesion area ± SEM are shown as graphs in the upper panel (A), representative sections stained with oil red O below (B).</p

    Successful reconstitution of peripheral blood cells by fetal liver cell transplantation.

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    <p>LDLR<sup>−/−</sup> mice (CD45.2-positive/CD45.1-negative, A) were lethally irradiated (2×450 cGy) and reconstituted with fetal liver cells of 6–8 week old CD45.1-positive/CD45.2-negative mice (B). After an interval of 4 weeks, peripheral blood cells were immunostained with CD45.1-PE and CD45.2-FITC (exemplary donors are shown in C and D) or CD45.1-PE in combination with CD19-PECy (B-cell marker, E), CD3-APC (T-cell marker, F), and CD11b-FITC (monocytic marker, G) antibodies and analyzed by FACS.</p

    TRAF6 deficiency does not alter lipid deposition in the abdominal aorta.

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    <p>Lethally irradiated 6 week old TRAF6<sup>+/+</sup>/LDLR<sup>−/−</sup> mice received TRAF6-deficient (hatched bars, N = 10) or competent fetal liver cells (white bars, N = 10), TRAF6<sup>+/−</sup>/LDLR<sup>−/−</sup> mice received TRAF6-deficient fetal liver cells (black bars, N = 10) only. Subsequently, all groups consumed high cholesterol diet (HCD) for 18 weeks. Abdominal aortas were fixed in formalin, pinned, and stained with oil red O to detect lipid deposition. Oil red O-positive staining in per cent of total area is shown as mean±SEM in the upper panel (A), representative images are shown below (B).</p

    TRAF6 deficiency does not alter plaque composition.

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    <p>Lethally irradiated 6 week old TRAF6<sup>+/+</sup>/LDLR<sup>−/−</sup> mice received TRAF6-deficient (hatched bars, N = 21) or competent fetal liver cells (white bars, N = 21), TRAF6<sup>+/−</sup>/LDLR<sup>−/−</sup> mice received TRAF6-deficient fetal liver cells (black bars, N = 22) only. Subsequently, all groups consumed high cholesterol diet (HCD) for 18 weeks. Sections of the aortic roots were analyzed for macrophage- (A), lipid- (B), smooth muscle cell- (C), collagen (D), and T cell-content (E). Mac-3-, oil-red-O-, α-actin-, picrosirius red, and CD4-positive staining in per cent of total wall area is displayed as mean±SEM.</p

    Weights, cholesterol-, and leukocyte levels before and after high cholesterol diet.

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    <p>Lethally irradiated 6 week old TRAF6<sup>+/+</sup>/LDLR<sup>−/−</sup> mice received TRAF6-deficient (hatched bars, N = 22) or competent fetal liver cells (white bars, N = 27), TRAF6<sup>+/−</sup>/LDLR<sup>−/−</sup> mice received TRAF6-deficient fetal liver cells (black bar, N = 23) only. Subsequently, all groups consumed high cholesterol diet (HCD) for 18 weeks. Weights (A), plasma cholesterol levels (B), triglycerides (C), and leukocyte counts (D) were taken before and after HCD.</p
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