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. 2021 Aug 26;9(5):1357–1367. doi: 10.1016/j.gendis.2021.08.005

Figure 1.

Figure 1

Ablation of RGS12 in macrophages does not affect the cartilage development in mice. (A) Generation of RGS12 cKO mice. RGS12 genomic locus, the floxed RGS12 targeting allele, the LysM-Cre transgene, and the recombinant RGS12 cKO allele. Exons are indicated by black boxes and numbered. Neo, neomycin resistance gene; loxP, loxP sites; Cre, Cre recombinase coding sequence. (B) Two-month-old female RGS12 cKO (LysM-Cre+; RGS12 fl/fl) mice show no growth retardation in comparison to WT (LysM-Cre+) mice (n = 10). (C) Measurement of body weight at 8 weeks shows no significant change (n = 10). ND: no difference (P > 0.05). (D) Measurement of body length at 8 weeks shows no significant change (n = 10). ND: no difference (P > 0.05). (E) BMMs derived from WT and RGS12 cKO were immunoblotted with an antibody against mouse RGS12. β-Actin was used as a loading control. ∗∗∗P < 0.001, vs. WT group, n = 5. (F) Sagittal sections of the knee joint of WT and RGS12 cKO mice at the age of 8 weeks (n = 10). Note that the Safranin O positive area showed no significant change. ND: no difference (P > 0.05). (G) Gene expression levels of IL1β, IL6, and TNFα in the cartilage tissue from WT and RGS12 KO mice were measured by RT-qPCR. Data are reported as means ± SEM (n = 5). ND: no difference (P > 0.05). (H) Gene expression levels of Col2 and Sox9 in the cartilage tissue from WT and RGS12 KO mice. Data are reported as means ± SEM (n = 5). ND: no difference (P > 0.05).