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. Author manuscript; available in PMC: 2019 May 21.
Published in final edited form as: Nature. 2018 Nov 21;563(7733):714–718. doi: 10.1038/s41586-018-0735-5

Figure 5. SLC16A1-mediated lactate release promotes an anti-inflammatory environment.

Figure 5.

(a-c) qPCR of Slc2a1, Slc16a1, and Sgk1 during distinct steps of efferocytosis. Supernatants from apoptotic cells, PtdSer-containing liposomes, or apoptotic cells (AC) were added to LR73 cells with or without cytochalasin D (1μM) for 4h, and qPCR performed. ***p < .001. (d) Lactate release from efferocytic phagocytes. LR73 cells (control or Slc16a1 siRNA) were incubated with apoptotic cells, washed, incubated an additional 4h, and lactate measured. ***p < .001. *p < .05. Data in a-d represent two independent experiments with 3–4 replicates per condition. (e) Schematic of supernatant preparation from LR73 phagocytes, adding supernatants to BMDMs, and analysis. (f) Determination of anti-inflammatory genes by qPCR. ***p < .001. Data represent two independent experiments with 2–3 replicates per condition. (g) Schematic of the upregulation and function of the SLC2A1-SGK1-SLC16A1 axis during efferocytosis.