Fig. 7: Inhibition of GPX4 sensitizes NRVMs to ferroptosis in the absence of cysteine. | Cell Death & Disease

Fig. 7: Inhibition of GPX4 sensitizes NRVMs to ferroptosis in the absence of cysteine.

From: Quantitative proteomic analyses reveal that GPX4 downregulation during myocardial infarction contributes to ferroptosis in cardiomyocytes

Fig. 7

a Cell viability of neonatal rat ventricular myocytes (NRVMs) treated with RSL3. NRVMs were treated with different concentrations of RSL3 for 24 h, and cell viability was analysed as described above. b NRVMs were incubated in cysteine- and methionine-deficient medium for 24 h. Glutathione levels were measured using a glutathione assay kit according to the manufacturer’s instructions and normalized to protein concentrations. n.d. = not determined. c RSL3-induced ferroptosis in NRVMs cultured in cysteine-depleted medium. NRVMs were incubated with normal DMEM or cysteine-depleted DMEM. After 24 h, cells were treated with 0.5 μM RSL3 for an additional 24 h, and cell viability was analysed as described above. The data are the mean ± s.d., n = 3, with **P < 0.01, ***P < 0.001 and n.s. = nonsignificant with a two-sided Student’s t-test. d siRNA-mediated knockdown of GPX4 in NRVMs. NRVMs were transfected with 20 nM GPX4 siRNA for 48 h and subjected to western blot analysis. e Effect of a combination of GPX4 knockdown and cysteine deprivation on ferroptosis in NRVMs. NRVMs were transfected with 20 nM siGPX4. After 24 h, the medium was replaced with cysteine-deficient medium with or without 1 μM Fer-1, and the cells were incubated for an additional 48 h. Cell viability was analysed as described above. The data are the mean ± s.d., n = 3, with **P < 0.01 and ***P < 0.001 with a two-sided Student’s t-test

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