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Macrophages with a deletion of thephosphoenolpyruvate carboxykinase 1(Pck1) gene
have a more proinflammatory phenotype.
Ko CW, Counihan D, Wu J, Hatzoglou M, Puchowicz MA, Croniger CM
Submitted Externally on 3/23/2018
The Journal of biological chemistry
Volume : Pages
293 : 3399 - 3409
Phosphoenolpyruvate carboxykinase (Pck1) is a metabolic enzyme that is integral
to the gluconeogenic and glyceroneogenic pathways. However, Pck1's role in
macrophage metabolism and function is unknown. Using stable isotopomer MS
analysis in a mouse model with a myeloid cell-specificPck1deletion, we show here
that this deletion increases the proinflammatory phenotype in macrophages.
Incubation of LPS-stimulated bone marrow-derived macrophages (BMDM) with
[U-13C]glucose revealed reduced13C labeling of citrate and malate and
increased13C labeling of lactate in Pck1-deleted bone marrow-derived
macrophages. We also found that the Pck1 deletion in the myeloid cells increases
reactive oxygen species (ROS). Of note, this altered macrophage metabolism
increased expression of the M1 cytokines TNFa, IL-1ß, and IL-6. We therefore
conclude thatPck1contributes to M1 polarization in macrophages. Our findings
provide important insights into the factors determining the macrophage
inflammatory response and indicate that Pck1 activity contributes to metabolic
reprogramming and polarization in macrophages.
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