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    Cell Signaling Technology Inc rabbit anti b catenin
    PPARγ in osteoblasts regulated sclerostin production to influence metabolism (A) qPCR analysis of Sost mRNA levels in the femur of male control and ΔPparg mice (n = 6–8 mice per genotype). (B) Quantification of serum sclerostin levels in male control and ΔPparg mice (n = 6–8 mice per genotype). (C and D) Sost mRNA levels (n = 6 mice per genotype, C) and serum sclerostin levels (n = 8–10 mice per genotype, D) were quantified in male control and ΔPparg mice fed a high fat diet (60% kcal from fat) from ages 4 to 16 weeks. (E and F) Sost mRNA levels (n = 6 mice per genotype, C) and serum sclerostin levels (n = 6–8 mice per genotype, D) were quantified in female control and ΔPparg mice. (G) qPCR analysis of Sost mRNA levels in cultures of control and ΔPparg primary osteoblasts after 14 days of differentiation (n = 11 samples per group). (H and I) qPCR analysis of Sost (H) and Axin2 (I) mRNA levels in Ocy454 cells 24 h after treatment with vehicle or rosiglitazone (n = 6 samples per group). (J) Western blot analysis of active, non-phosphorylated <t>b-catenin</t> and total b-catenin in the iWAT of 16-week-old male control and ΔPparg mice. (K and L) qPCR analysis of Axin2 and Ctnnb1 mRNA levels in the iWAT of control and ΔPparg mice fed a chow diet (K) or a high fat diet from ages 4 to 16 weeks (n = 5–6 mice per genotype). (M–Y) 8-week-old control and ΔPparg mice were injected with AAV-8 constructs directing the expression of Sost or GFP and then aged for an additional 8 weeks. (M) Serum sclerostin levels (n = 8–10 mice per group). (N) Western blot analysis of active, non-phosphorylated β-catenin and total β-catenin in the iWAT. (O) Weight gained during the 8-week experiment (n = 8–10 mice per group). (P and Q) Representative microCT images of the distal femur and quantification of trabecular bone volume (n = 8–10 mice per group). (R) iWAT mass (n = 8–10 mice per group). (S) Representative hematoxylin and eosin histological sections of iWAT (10× original magnification). (T and U) qPCR analysis of Fasn and Ucp1 mRNA levels in iWAT (n = 8–9 mice per group). (V) Random fed blood glucose (n = 8–10 mice per group). (W) Serum insulin levels (n = 8–10 mice per group). (X and Y) Insulin tolerance testing and area under the curve analysis (n = 8–10 mice per group). Data presented as mean and standard deviation. ∗, p < 0.05. Data were analyzed by unpaired Student’s t test or Anova followed by Tukey’s multiple comparison post hoc test.
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    1) Product Images from "Peroxisome proliferator activated receptor-γ in osteoblasts controls bone formation and fat mass by regulating sclerostin expression"

    Article Title: Peroxisome proliferator activated receptor-γ in osteoblasts controls bone formation and fat mass by regulating sclerostin expression

    Journal: iScience

    doi: 10.1016/j.isci.2023.106999

    PPARγ in osteoblasts regulated sclerostin production to influence metabolism (A) qPCR analysis of Sost mRNA levels in the femur of male control and ΔPparg mice (n = 6–8 mice per genotype). (B) Quantification of serum sclerostin levels in male control and ΔPparg mice (n = 6–8 mice per genotype). (C and D) Sost mRNA levels (n = 6 mice per genotype, C) and serum sclerostin levels (n = 8–10 mice per genotype, D) were quantified in male control and ΔPparg mice fed a high fat diet (60% kcal from fat) from ages 4 to 16 weeks. (E and F) Sost mRNA levels (n = 6 mice per genotype, C) and serum sclerostin levels (n = 6–8 mice per genotype, D) were quantified in female control and ΔPparg mice. (G) qPCR analysis of Sost mRNA levels in cultures of control and ΔPparg primary osteoblasts after 14 days of differentiation (n = 11 samples per group). (H and I) qPCR analysis of Sost (H) and Axin2 (I) mRNA levels in Ocy454 cells 24 h after treatment with vehicle or rosiglitazone (n = 6 samples per group). (J) Western blot analysis of active, non-phosphorylated b-catenin and total b-catenin in the iWAT of 16-week-old male control and ΔPparg mice. (K and L) qPCR analysis of Axin2 and Ctnnb1 mRNA levels in the iWAT of control and ΔPparg mice fed a chow diet (K) or a high fat diet from ages 4 to 16 weeks (n = 5–6 mice per genotype). (M–Y) 8-week-old control and ΔPparg mice were injected with AAV-8 constructs directing the expression of Sost or GFP and then aged for an additional 8 weeks. (M) Serum sclerostin levels (n = 8–10 mice per group). (N) Western blot analysis of active, non-phosphorylated β-catenin and total β-catenin in the iWAT. (O) Weight gained during the 8-week experiment (n = 8–10 mice per group). (P and Q) Representative microCT images of the distal femur and quantification of trabecular bone volume (n = 8–10 mice per group). (R) iWAT mass (n = 8–10 mice per group). (S) Representative hematoxylin and eosin histological sections of iWAT (10× original magnification). (T and U) qPCR analysis of Fasn and Ucp1 mRNA levels in iWAT (n = 8–9 mice per group). (V) Random fed blood glucose (n = 8–10 mice per group). (W) Serum insulin levels (n = 8–10 mice per group). (X and Y) Insulin tolerance testing and area under the curve analysis (n = 8–10 mice per group). Data presented as mean and standard deviation. ∗, p < 0.05. Data were analyzed by unpaired Student’s t test or Anova followed by Tukey’s multiple comparison post hoc test.
    Figure Legend Snippet: PPARγ in osteoblasts regulated sclerostin production to influence metabolism (A) qPCR analysis of Sost mRNA levels in the femur of male control and ΔPparg mice (n = 6–8 mice per genotype). (B) Quantification of serum sclerostin levels in male control and ΔPparg mice (n = 6–8 mice per genotype). (C and D) Sost mRNA levels (n = 6 mice per genotype, C) and serum sclerostin levels (n = 8–10 mice per genotype, D) were quantified in male control and ΔPparg mice fed a high fat diet (60% kcal from fat) from ages 4 to 16 weeks. (E and F) Sost mRNA levels (n = 6 mice per genotype, C) and serum sclerostin levels (n = 6–8 mice per genotype, D) were quantified in female control and ΔPparg mice. (G) qPCR analysis of Sost mRNA levels in cultures of control and ΔPparg primary osteoblasts after 14 days of differentiation (n = 11 samples per group). (H and I) qPCR analysis of Sost (H) and Axin2 (I) mRNA levels in Ocy454 cells 24 h after treatment with vehicle or rosiglitazone (n = 6 samples per group). (J) Western blot analysis of active, non-phosphorylated b-catenin and total b-catenin in the iWAT of 16-week-old male control and ΔPparg mice. (K and L) qPCR analysis of Axin2 and Ctnnb1 mRNA levels in the iWAT of control and ΔPparg mice fed a chow diet (K) or a high fat diet from ages 4 to 16 weeks (n = 5–6 mice per genotype). (M–Y) 8-week-old control and ΔPparg mice were injected with AAV-8 constructs directing the expression of Sost or GFP and then aged for an additional 8 weeks. (M) Serum sclerostin levels (n = 8–10 mice per group). (N) Western blot analysis of active, non-phosphorylated β-catenin and total β-catenin in the iWAT. (O) Weight gained during the 8-week experiment (n = 8–10 mice per group). (P and Q) Representative microCT images of the distal femur and quantification of trabecular bone volume (n = 8–10 mice per group). (R) iWAT mass (n = 8–10 mice per group). (S) Representative hematoxylin and eosin histological sections of iWAT (10× original magnification). (T and U) qPCR analysis of Fasn and Ucp1 mRNA levels in iWAT (n = 8–9 mice per group). (V) Random fed blood glucose (n = 8–10 mice per group). (W) Serum insulin levels (n = 8–10 mice per group). (X and Y) Insulin tolerance testing and area under the curve analysis (n = 8–10 mice per group). Data presented as mean and standard deviation. ∗, p < 0.05. Data were analyzed by unpaired Student’s t test or Anova followed by Tukey’s multiple comparison post hoc test.

    Techniques Used: Western Blot, Injection, Construct, Expressing, Standard Deviation


    Figure Legend Snippet:

    Techniques Used: Plasmid Preparation, Recombinant, SYBR Green Assay, Quantitation Assay, Enzyme-linked Immunosorbent Assay, Software

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