Skip to main content
. 2022 Jan 4;6(1):108–120. doi: 10.1182/bloodadvances.2021004640

Figure 4.

Figure 4.

SBDS deficiency within BM niche cells diminishes gene expression downstream of IGF-1 signaling. (A) Protein expression of IGF-1, IGFBP-2, and IGFBP-3 in BM supernatants harvested from Mx1CreSBDSExc and control mice at baseline and 48 hours after 1100 cGy TBI (n ≥ 5 per group). *P < .05; **P < .01; Student t-test. (B) GSEA plot showing statistically significant alterations in IGF-1 signaling pathway gene expression in BM stromal cells from Mx1CreSBDSExc mice vs controls 24 hours after TBI (n = 5 per group). (C) Upregulation of upstream and downregulation of downstream signaling genes within the IGF-1 pathway in the BM stromal cells of irradiated Mx1CreSBDSExc mice compared with controls. *P < .05; **P < .01; ***P < .001; DESeq2 statistical test. (D) qPCR validation confirms that BM niche cells from Mx1CreSbdsExc mice (n = 3) at 24 hours after 1100 cGy TBI show increased expression of IGF-1 factor genes Igfbp2 and Igfbp3, along with decreased expression of downstream IGF-1 signaling pathway genes, including Raf1 and Fos, compared with irradiated controls (n = 4). *P < .05; **P < .01; Student t-test.