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. 2018 Apr 30;128(6):2339–2355. doi: 10.1172/JCI96208

Figure 8. Spry1 is a target of HIF2A in QSCs.

Figure 8

(A) Luciferase assays showed that stabilized expression of HIF2A (HIF2ATM), but not HIF1A (HIF1ATM), increased the promoter activities of Spry1 and Atp7a (a known HIF2A target). In contrast, HIF1A, but not HIF2A, transactivated the Pdk3 promoter. (B) ChIP-qPCR indicated that HIF2A bound the promoters of Spry1 and Cav1 (a known HIF2A target), but not the Pdk3 promoter, in QSCs in vivo. (C) RT-qPCR revealed that HIF2A ablation in QSCs in vivo reduced the mRNA levels of Hif2a, Spry1, Calcr, and Cd36. (D) RT-qPCR indicated that 2 HIF2A shRNAs reduced the mRNA levels of Hif2a and Spry1 as well as of 2 known HIF2A targets, Atp7a and Cxcl12, in C2C12 myoblasts. (E) RT-qPCR revealed that HIF-c2 treatment decreased mRNA levels of the HIF2A targets Spry1, Atp7a, and Cxcl12 in C2C12 myoblasts. (F) RT-qPCR indicated that HIF2ATM increased the mRNA levels of Spry1 as well as of 2 known HIF2A targets, Atp7a and Cxcl12, in C2C12 myoblasts. *P < 0.05, **P < 0.01, and ***P < 0.005, by 2-sided Student’s t test. Data represent the mean ± SEM.