BioProject

Ferroptosis, a non-apoptotic form of programmed cell death, is triggered by oxidative stress in cancer, heat stress in plants and hemorrhagic stroke. More...

Ferroptosis, a non-apoptotic form of programmed cell death, is triggered by oxidative stress in cancer, heat stress in plants and hemorrhagic stroke. A homeostatic transcriptional response to ferroptotic stimuli is unknown. We show that neurons respond to ferroptotic stress by induction of a transcriptional adaptive response. Pharmacological selenium (Se) augments mitochondrial and nuclear GPX4 and other genes in this transcriptional program, the selenome, via coordinated activation of the transcription factors TFAP2c and Sp1, to protect neurons. This RNA seq data uses primary cortical neurons in cultures treated with either homocysteic acid (HCA), which induces ferroptosis and/or Se, which augments the adaptation to ferroptosis. Both protective (1mM Se) and non-protective (0.1mM Se) of selenium are used. Cells are collected after 6 hours when the transcriptional response is observed. Overall design: Primary cortical neurons are plated from E15 mouse pups for 24 hours. Then either ferroptosis inhibitor HCA (5mM) and/or sodium selenite (0-1uM) is added to the cultures in bath. Cultures are washed with PBS and scraped for RNA collection. RNA is purified and quality measured. RNA was depleted with Ribo-zero gold and RNA seq was done using Hi seq 4000. Less...