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. Author manuscript; available in PMC: 2022 Feb 19.
Published in final edited form as: Cell Chem Biol. 2021 Feb 10;28(8):1169–1179.e6. doi: 10.1016/j.chembiol.2021.01.008

Figure 2. Metabolism of Me-lyso-PSs by carboxylesterases and the pro-inflammatory activity of Me-lyso-PSs in macrophages.

Figure 2

(A) Top: The enzymatic reaction for metabolism (hydrolysis) of Me-lyso-PSs to the corresponding lyso-PSs catalyzed by carboxylesterases; Bottom: Extracted ion chromatograms from a LC-MS analysis of (R)-2b (C12:0) ([M-H]– = 454.221), (R)-2e (C18:0) ([M-H]– = 538.315) and (R)-2h (C24:0) ([M-H]– = 622.409) showing the complete conversion of the parent compound (Me-lyso-PS) to the corresponding lyso-PS (loss of 14 Da) following treatment with active (blue trace), but not denatured (red trace), porcine liver carboxylesterase (0.1 U, 15 mins, 37 °C). In these assays, 100 㭜g of the (R)-Me-lyso-PS was used, and a no-enzyme standard only control (dotted black trace) was also included for the same treatment. This LC-MS experiment was done twice for each of the (R)-Me-lyso-PS, with reproducible result each time. (B) Secreted TNF-α and IL-6 from PPM harvested from wild type (+/+) or ABHD12 knockout (–/–) mice following treatment with vehicle (DMSO) or lipopolysaccharide (LPS) or (R)-2a-h (1 㭜M, 4 hours, 37 °C); *p < 0.05, **p < 0.01, and ***p < 0.001 versus (+/+) group by Student’s two-tailed t-test.