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. Author manuscript; available in PMC: 2023 Mar 1.
Published in final edited form as: Sci Signal. 2021 Nov 2;14(707):eabd4077. doi: 10.1126/scisignal.abd4077

Fig. 6. Absence of TRPV4 does not perturb BMDM receptors known to be involved in the FBR or FBGC formation.

Fig. 6.

(A) Representative images showing CD36, TRPV4, and nuclei (DAPI) in WT and Trpv4−/− BMDMs after treatment with IL-4 + GM-CSF or untreated. Cells were also stained with isotype control IgGs. Scale bars, 20 μm. n = 3 independent experiments and 10 cells per condition. (B) Representative log plot of flow cytometric data showing cell surface abundance of CD36 in WT and Trpv4−/− BMDMs and TRPV4 in WT BMDMs after incubation with IL-4 + GM-CSF for 24 hours. (C) Quantification of data from (B). n = 3 independent experiments and 20,000 cells per condition; Student’s t test. (D) Immunoblotting and quantification of the BMDM receptors CD36, ECAD1, SRA-1, TLR4, and CD47 at 24 and 48 hours after treatment of WT and Trpv4−/− BMDMs with IL-4 + GM-CSF. GAPDH is a loading control. n = 3 biological replicates. Two-way ANOVA followed by Bonferroni test. A.U., arbitrary units.