Regulation of ATP13A2 via PHD2-HIF1α Signaling Is Critical for Cellular Iron Homeostasis: Implications for Parkinson's Disease

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Figure 3.
Figure 3.

Reductions in PHD2 activity results in increases in expression of ATP13A2. A, RT-PCR analysis of ATP13A2 expression levels in mesencephalic cultures isolated from PHD2 control mice in the presence of pharmacological PHD2 inhibition via IOX2 demonstrates increased expression versus untreated controls. Data are reported as fold change. *p < 0.01 versus controls, unpaired t test. B, C, RT-PCR analyses of ATP13A2 levels in OB (B) and ST (C) tissues isolated from genetic PHD2 knock-out versus PHD2 control mice demonstrates upregulation gene expression in the context of in vivo reductions in DAergic PHD2 levels. The HIF1α target gene HO-1 was included as a positive control. Data are reported as fold change. *p < 0.01 versus controls, unpaired t test. D, Western blot analysis of ATP13A2 and HO-1 levels in striatal tissues isolated from PHD2 knockdowns (KDs) versus control mice demonstrates significant elevations in protein levels. Data are reported as percentage PHD2 control normalized to actin; *p < 0.01 versus PHD2, #p < 0.01 versus PHD2, unpaired t test. E, Western blot analysis of ATP13A2 levels in striatal tissues isolated from PHD1 and PHD3 KDs versus control mice demonstrates no significant change in protein levels. Data are reported as percentage PHD1 and PHD3 control normalized to actin, unpaired t test.

  1. The Journal of Neuroscience vol. 36 no. 4 1086-1095
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