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• W1976970110 abstract "BackgroundMacrophages are heterogeneous in nature and may play different roles in atherosclerosis progression. Previous studies have shown that macrophages can vary in their function depending on the specific nature of the cytokine environment. We sought to evaluate the ability of different monocyte-derived macrophage (MDM) sub-phenotypes to maintain cholesterol homeostasis.MethodsPrimary human monocytes were differentiated into macrophages and subsequently treated with cytokines including interleukin-4 and interleukin-13 (IL4/13), interferon gamma and tumor necrosis factor alpha (IFNg/TNFa), or interleukin-10 to induce unique functional phenotypes. Oxidized LDL (oxLDL) cellular association (4 hours) and cholesterol accumulation (24 hours) were evaluated and compared to untreated controls. Expression of targets likely to be involved in oxLDL metabolism such as CD36, SR-AI, and peroxisome proliferator-actived receptor gamma (PPARg) were measured.ResultsIFNg/TNFa treated MDMs showed a 86% reduction of oxLDL cellular association (P < 0.05) which may be partially explained by the 49% reduction in both CD36 mRNA and protein (P < 0.01, P < 0.05). IFNg/TNFa caused a 33% decrease in PPARg protein expression (P < 0.01), a transcription factor known to positively regulate CD36. IL4/13 treatment resulted in a 49% and 67% reduction in CD36 mRNA and protein expression respectively (P < 0.01, P < 0.01), but no significant decreases in oxLDL cellular association were observed. IFNg/TNFa also caused a 33% decrease in total cholesterol accumulation (P < 0.05) which was accompanied by a 50% and 81% reduction in CD36 mRNA and protein respectively (P < 0.01 P < 0.001). The reduction in CD36 expression seen with IL4/13 treatment during the oxLDL cellular association assay was not present during the cholesterol accumulation assay. No changes in SR-AI mRNA were observed amongst any of the cytokine treatments in either assay. In addition, the effects of the IL10 treatment did not differ greatly from the untreated control for both of the functional assays.ConclusionMacrophages treated with IFNg/TNFa have distinct changes in cholesterol metabolism associated with cholesterol accumulation and oxLDL cellular association compared to untreated cells. These differences are likely related in part to the observed changes in the expression CD36 and PPARg. More detailed mechanisms are currently under investigation. BackgroundMacrophages are heterogeneous in nature and may play different roles in atherosclerosis progression. Previous studies have shown that macrophages can vary in their function depending on the specific nature of the cytokine environment. We sought to evaluate the ability of different monocyte-derived macrophage (MDM) sub-phenotypes to maintain cholesterol homeostasis. Macrophages are heterogeneous in nature and may play different roles in atherosclerosis progression. Previous studies have shown that macrophages can vary in their function depending on the specific nature of the cytokine environment. We sought to evaluate the ability of different monocyte-derived macrophage (MDM) sub-phenotypes to maintain cholesterol homeostasis. MethodsPrimary human monocytes were differentiated into macrophages and subsequently treated with cytokines including interleukin-4 and interleukin-13 (IL4/13), interferon gamma and tumor necrosis factor alpha (IFNg/TNFa), or interleukin-10 to induce unique functional phenotypes. Oxidized LDL (oxLDL) cellular association (4 hours) and cholesterol accumulation (24 hours) were evaluated and compared to untreated controls. Expression of targets likely to be involved in oxLDL metabolism such as CD36, SR-AI, and peroxisome proliferator-actived receptor gamma (PPARg) were measured. Primary human monocytes were differentiated into macrophages and subsequently treated with cytokines including interleukin-4 and interleukin-13 (IL4/13), interferon gamma and tumor necrosis factor alpha (IFNg/TNFa), or interleukin-10 to induce unique functional phenotypes. Oxidized LDL (oxLDL) cellular association (4 hours) and cholesterol accumulation (24 hours) were evaluated and compared to untreated controls. Expression of targets likely to be involved in oxLDL metabolism such as CD36, SR-AI, and peroxisome proliferator-actived receptor gamma (PPARg) were measured. ResultsIFNg/TNFa treated MDMs showed a 86% reduction of oxLDL cellular association (P < 0.05) which may be partially explained by the 49% reduction in both CD36 mRNA and protein (P < 0.01, P < 0.05). IFNg/TNFa caused a 33% decrease in PPARg protein expression (P < 0.01), a transcription factor known to positively regulate CD36. IL4/13 treatment resulted in a 49% and 67% reduction in CD36 mRNA and protein expression respectively (P < 0.01, P < 0.01), but no significant decreases in oxLDL cellular association were observed. IFNg/TNFa also caused a 33% decrease in total cholesterol accumulation (P < 0.05) which was accompanied by a 50% and 81% reduction in CD36 mRNA and protein respectively (P < 0.01 P < 0.001). The reduction in CD36 expression seen with IL4/13 treatment during the oxLDL cellular association assay was not present during the cholesterol accumulation assay. No changes in SR-AI mRNA were observed amongst any of the cytokine treatments in either assay. In addition, the effects of the IL10 treatment did not differ greatly from the untreated control for both of the functional assays. IFNg/TNFa treated MDMs showed a 86% reduction of oxLDL cellular association (P < 0.05) which may be partially explained by the 49% reduction in both CD36 mRNA and protein (P < 0.01, P < 0.05). IFNg/TNFa caused a 33% decrease in PPARg protein expression (P < 0.01), a transcription factor known to positively regulate CD36. IL4/13 treatment resulted in a 49% and 67% reduction in CD36 mRNA and protein expression respectively (P < 0.01, P < 0.01), but no significant decreases in oxLDL cellular association were observed. IFNg/TNFa also caused a 33% decrease in total cholesterol accumulation (P < 0.05) which was accompanied by a 50% and 81% reduction in CD36 mRNA and protein respectively (P < 0.01 P < 0.001). The reduction in CD36 expression seen with IL4/13 treatment during the oxLDL cellular association assay was not present during the cholesterol accumulation assay. No changes in SR-AI mRNA were observed amongst any of the cytokine treatments in either assay. In addition, the effects of the IL10 treatment did not differ greatly from the untreated control for both of the functional assays. ConclusionMacrophages treated with IFNg/TNFa have distinct changes in cholesterol metabolism associated with cholesterol accumulation and oxLDL cellular association compared to untreated cells. These differences are likely related in part to the observed changes in the expression CD36 and PPARg. More detailed mechanisms are currently under investigation. Macrophages treated with IFNg/TNFa have distinct changes in cholesterol metabolism associated with cholesterol accumulation and oxLDL cellular association compared to untreated cells. These differences are likely related in part to the observed changes in the expression CD36 and PPARg. More detailed mechanisms are currently under investigation." @default.
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• W1976970110 title "070 Macrophages treated with interferon gamma and tumor necrosis factor alpha exhibit decreased cholesterol accumulation and are associated with decreased CD36 and peroxisome proliferator-activated receptor gamma expression" @default.
• W1976970110 doi "https://doi.org/10.1016/j.cjca.2011.07.063" @default.
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