Fig. 3: Generation and characterization of tamoxifen-inducible, SMC-specific GPR153 knockout mice (iSM-G153-KOs). | Nature Communications

Fig. 3: Generation and characterization of tamoxifen-inducible, SMC-specific GPR153 knockout mice (iSM-G153-KOs).

From: Orphan receptor GPR153 facilitates vascular damage responses by modulating cAMP levels, YAP/TAZ signaling, and NF-κB activation

Fig. 3

A Design of the floxed Gpr153 allele. B Gpr153 knockout efficiency was determined by qRT-PCR in the cleaned aortic media of tamoxifen-treated control and iSM-G153-KO mice (data normalized to Gapdh, control set to 1, n = 5–6). C, D EdU incorporation was determined in cells cultured for 2 weeks from digested aortas of control and iSM-G153-KOs (both bred to the mTmG reporter line; SMCs are EGFP-expressing): C representative photomicrographs; D statistical evaluation (n = 3–4). E, F qRT-PCR in the cleaned tunica media of carotid arteries from control mice and iSM-G153-KOs (data normalized to Gapdh and control set to 1, n = 10). G, H Immunoblot analysis of carotid arteries (cleaned tunica media) from control mice and iSM-G153-KOs: G representative blots; H densitometric analysis of signal strength normalized to loading control GAPDH (n = 5–6). I, J Dose–response curves for the indicated vasoconstrictors were determined by wire myography in mesenteric arteries from control mice and iSM-G153-KOs (data normalized to reference contractions elicited by 60 mM KCl; n = 10–14). Data are means ± SEM; comparisons between genotypes were performed using unpaired two-sided t test (B, D, E), two-way ANOVA and Sidak’s multiple comparisons test (F, H–J). n number of individual mice; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

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