Fig. 2: mTORC1 signaling induces NRF1 during OGD/R. | Cell Death Discovery

Fig. 2: mTORC1 signaling induces NRF1 during OGD/R.

From: NRF1 coordinates mitochondrial adaptations to dampen intracellular ROS and inflammatory responses during ischemia reperfusion

Fig. 2: mTORC1 signaling induces NRF1 during OGD/R.

A, B BMDMs were treated with OGD followed by different durations of reoxygenation. Nfe2l1 transcript was analyzed by qRT-PCR (A) and NRF1 proteins levels in cytosolic and nuclear fractions was analyzed by WB (B). C BMDMs were treated with OGD followed by different durations of reoxygenation +/− H2O2 treatment during reoxygenation. NRF1 proteins levels in cytosolic and nuclear fractions was analyzed by WB. D BMDMs were treated with OGD followed by different durations of reoxygenation. NRF1 protein levels and mTORC1 signaling were assessed by WB. E BMDMs were subject to different durations of OGD followed by 1 h reoxygenation. NRF1 levels and mTORC1 signaling were assessed by WB. F BMDMs were subject to OGD/R +/− mTOR inhibitor (rapamycin, 400 nM) or S6K inhibitor (PF-4708671, 10 μM) during reoxygenation as indicated. NRF1 levels and mTORC1 signaling were assessed by WB. G Top, mouse model of ischemia and reperfusion injury induced acute kidney injury (IRI-AKI). Bottom, NRF1 MFI in F4/80+ CD11b+ cells of kidneys subject to IRI-AKI or sham; quantitation and representative histogram are shown. Statistical test by one-way ANOVA and 2-tailed samples t-test (n = 3–6 and representative of 3–6 independent experiments, n.s. no significance, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001).

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