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. Author manuscript; available in PMC: 2022 Sep 28.
Published in final edited form as: Nat Cardiovasc Res. 2022 Mar 28;1(4):344–360. doi: 10.1038/s44161-022-00027-7

Extended Data Fig. 1. Knockout of Trpm2 in Apoe−/− mice.

Extended Data Fig. 1

(a) Representative PCR genotyping results showing a 514bp and 740 bp products for WT and M2KO mice. (b) Representative WB analysis of TRPM2 expression in macrophages isolated from Apoe single knockout (WT (n=3)) and Apoe / Trpm2 double knockout (M2KO (n=3)) mice (c-e) Representative recording (c, I-V curve; d, time-current trace) and quantification of TRPM2 current in macrophages isolated from Apoe single knockout (WT) and Apoe / Trpm2 double knockout (M2KO) mice. ACA is a TRPM2 blocker. (***: p < 0.001; unpaired t test; mean ± SEM) (f) Graphic illustration showing the atherosclerotic area chosen for taking images of F4/80&CD80 staining in Fig 1i and Fig 3h. (g) Representative WB analysis of TRPM2 expression in macrophages isolated from Trpm2fl/flCd11b-cre− (n=3) and Trpm2fl/flCd11b-cre+ mice (n=3) with Apoe knockout. (h, i) Representative recording and quantification of TRPM2 current in macrophages isolated from Trpm2fl/flCd11b-cre− and Trpm2fl/flCd11b-cre+ mice with Apoe knockout.