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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. 5. TRPM2 is required for CD36 activation in macrophages induced by TSP1.

Extended Data Fig. 5

(a, b) Representative WB analysis of TRPM2 expression in macrophages isolated from WT mice with or without the treatment of TSP1 (10 μg/ml) for 24 h (n=6/group). (c, d) 30-min TSP1 (10 μg/ml) treatment induce the activation of CD36 signaling without upregulating CD36 expression. Representative WB analysis of CD36, pFyn, pJNK and pp38 expression in macrophages after TSP1 treatment for 30 min (n=6/group). (e, f) NADPH oxidase inhibitor apocynin does not inhibit CD36 activation induced by 24-h TSP1 (10 μg/ml) treatment in macrophages isolated from wild-type (WT) mice. Representative WB analysis of CD36, pFyn, pJNK and pp38 expression in macrophages after TSP1 treatment for 24 h. (g) A set of original Fura-2 real time recording traces without normalization during TSP1 treatment as in Fig 5g. (h, i) Trpm2 deletion does not influence the production of MCP1/MIF in endothelial cells isolated from aorta in response to 24-h TSP1 (10 μg/ml) treatment. Representative WB analysis of MCP1 and MIF expression in endothelial cells after TSP1 treatment for 24 h (n=6/group). (ns: no statistical significance; *: p < 0.05; **: p < 0.01; ***: p < 0.001; ANOVA, two-tailed, Bonferroni’s test; mean ± SEM).