HCMV infection downregulates GPX4 and stimulates lipid peroxidation but does not induce ferroptosis Figure 1

FIG 1 HCMV differentially regulates GPX4 and FSP1 during infection. (A) Lipid peroxidation measured with C11 BODIPY FITC fluorescence shift in MRC-5 cells either uninfected (0 hpi) or TB40/E-WT (MOI = 3) infected at 24, 48, 72, 96, and 120 hpi. Lipid peroxidation is shown relative to uninfected cells. Results are from two individual experiments, n = 6. (B) Model depicting the pathways of GPX4 and FSP1 to reduce lipid peroxidation and regulate ferroptosis. (C) Western blot analysis of lysates from uninfected MRC5 cells or MRC5 cells infected with TB40/E-WT (as in [A]) and harvested at 24, 48, 72, 96, and 120 hours. Blots were probed for GPX4, FSP1, IE2, pp28, and p115 as a loading control. The values under the GPX4 and FSP1 blots denote quantification of each GPX4 or FSP1 band in the blot, relative to the GPX4 or FSP1 band in the uninfected cells at 24 hours, respectively. For the above panels, * indicates P < 0.05 and ns = not signific