Namgaladze 2014 Biochim Biophys Acta: Difference between revisions
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{{Publication | {{Publication | ||
|title=Namgaladze D, BrΓΌne B (2014) | |title=Namgaladze D, BrΓΌne B (2014) Fatty acid oxidation is dispensable for human macrophage IL-4-induced polarization. Biochim Biophys Acta 1841:1329-35. | ||
|info=[https://pubmed.ncbi.nlm.nih.gov/24960101/ PMID:24960101] | |info=[https://pubmed.ncbi.nlm.nih.gov/24960101/ PMID:24960101] | ||
|authors=Namgaladze D, BrΓΌne B | |authors=Namgaladze D, BrΓΌne B | ||
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|abstract=Macrophage polarization elicits various metabolic alterations which in turn influence the polarized phenotype. Activation of glycolytic metabolism accompanies and supports macrophage pro-inflammatory M1 polarization. In contrast, M2 polarization of murine macrophages in response to the Th2 cytokine interleukin-4 (IL-4) was linked to the up-regulation of mitochondrial oxidative metabolism and fatty acid oxidation (FAO), which was necessary for coining an IL-4-polarized phenotype. Here we investigated whether similar mechanisms operate in human macrophages stimulated with IL-4. IL-4 causes only moderate changes of mitochondrial oxidative metabolism and FAO, correlating with an unaltered expression of peroxisome proliferator-activated receptor-Ξ³ coactivator 1 Ξ±/Ξ² (PGC-1Ξ±/Ξ²), the master transcriptional regulators of mitochondrial biogenesis. Furthermore, attenuating FAO had no effect on IL-4-induced polarization-associated gene expression. Apparently, FAO is dispensable for IL-4-induced polarization of human macrophages, pointing to fundamental differences in the metabolic requirements of macrophage phenotype alterations between mice and humans. | |abstract=Macrophage polarization elicits various metabolic alterations which in turn influence the polarized phenotype. Activation of glycolytic metabolism accompanies and supports macrophage pro-inflammatory M1 polarization. In contrast, M2 polarization of murine macrophages in response to the Th2 cytokine interleukin-4 (IL-4) was linked to the up-regulation of mitochondrial oxidative metabolism and fatty acid oxidation (FAO), which was necessary for coining an IL-4-polarized phenotype. Here we investigated whether similar mechanisms operate in human macrophages stimulated with IL-4. IL-4 causes only moderate changes of mitochondrial oxidative metabolism and FAO, correlating with an unaltered expression of peroxisome proliferator-activated receptor-Ξ³ coactivator 1 Ξ±/Ξ² (PGC-1Ξ±/Ξ²), the master transcriptional regulators of mitochondrial biogenesis. Furthermore, attenuating FAO had no effect on IL-4-induced polarization-associated gene expression. Apparently, FAO is dispensable for IL-4-induced polarization of human macrophages, pointing to fundamental differences in the metabolic requirements of macrophage phenotype alterations between mice and humans. | ||
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{{Template:Cited by Silva 2021 MitoFit Etomoxir}} | |||
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Latest revision as of 08:53, 6 July 2021
Namgaladze D, BrΓΌne B (2014) Fatty acid oxidation is dispensable for human macrophage IL-4-induced polarization. Biochim Biophys Acta 1841:1329-35. |
Namgaladze D, BrΓΌne B (2014) Biochim Biophys Acta
Abstract: Macrophage polarization elicits various metabolic alterations which in turn influence the polarized phenotype. Activation of glycolytic metabolism accompanies and supports macrophage pro-inflammatory M1 polarization. In contrast, M2 polarization of murine macrophages in response to the Th2 cytokine interleukin-4 (IL-4) was linked to the up-regulation of mitochondrial oxidative metabolism and fatty acid oxidation (FAO), which was necessary for coining an IL-4-polarized phenotype. Here we investigated whether similar mechanisms operate in human macrophages stimulated with IL-4. IL-4 causes only moderate changes of mitochondrial oxidative metabolism and FAO, correlating with an unaltered expression of peroxisome proliferator-activated receptor-Ξ³ coactivator 1 Ξ±/Ξ² (PGC-1Ξ±/Ξ²), the master transcriptional regulators of mitochondrial biogenesis. Furthermore, attenuating FAO had no effect on IL-4-induced polarization-associated gene expression. Apparently, FAO is dispensable for IL-4-induced polarization of human macrophages, pointing to fundamental differences in the metabolic requirements of macrophage phenotype alterations between mice and humans.
Cited by
- Silva et al (2021) Off-target effect of etomoxir on mitochondrial Complex I. MitoFit Preprints 2021. (in preparation)
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MitoFit 2021 Etomoxir