Fig. 2: NGFR is significantly upregulated in skeletal cells with committed osteochondral fates compared to progenitor cells at earlier stages. | Nature Communications

Fig. 2: NGFR is significantly upregulated in skeletal cells with committed osteochondral fates compared to progenitor cells at earlier stages.

From: Nerve growth factor receptor limits inflammation to promote remodeling and repair of osteoarthritic joints

Fig. 2

a, b Western results of NGFR in mouse cells (a) and in multiple human cell lines and RCS cells (b). n = 3 independent experiments. c Perturbations of NGFR validated the anti-NGFR antibody and confirmed NGFR proteins in C2C12. sg single guide RNA for CRISPR to mutate Ngfr. CRISPRa indicates CRISPR-mediated transcriptional activation of Ngfr. Control is the empty vector for CRISPRa. Note that sg1 targeting the promoter increased NGFR expression. n = 3 independent experiments. d TrkA had no detectable protein levels in skeletal cells. * Denotes non-specific bands detected. n = 3 independent experiments. e Ngfr mRNAs were markedly increased in mouse articular chondrocytes (AC), E14.5 limb bud cells, and C2C12 cells, compared to C3H10T1/2, ATDC5, and CD45- BMSCs. Data are presented as mean values ± SD. n = 3 independent experiments. One-way ANOVA. f, g NGFR mRNAs were significantly higher in human osteoblastic cell lines (hFOB1.19 and Saos-2) than in human mesenchymal stem cells (hMSC), whereas TrkA levels are significantly lower than NGFR in all examined cells. Data are presented as mean values ± SD. n = 3 independent experiments. One-way ANOVA. h, i NGFR proteins decreased with the dedifferentiation of committed skeletal cells induced by repeated passages. n = 3. *p < 0.05, **p < 0.01, ****p < 0.0001. Source data are provided as a Source Data file.

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