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Sub-lethal stimulation of ferroptosis leads to trophoblast dysfunction

ABSTRACT: Sub-lethal stimulation of ferroptosis leads to trophoblast dysfunction

PROVIDER: PRJNA615850 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11433753_1.fastq.gz	Fastqsanger.gz
	SRR11433753_2.fastq.gz	Fastqsanger.gz
	SRR11433754_1.fastq.gz	Fastqsanger.gz
	SRR11433754_2.fastq.gz	Fastqsanger.gz
	SRR11433755_1.fastq.gz	Fastqsanger.gz

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Sub-lethal stimulation of ferroptosis leads to trophoblast dysfunction

Project description:Ferroptosis is a recently identified program of regulated cell death, defined by excessive accumulation of hydroperoxy-arachidonoyl (C20:4)- or adrenoyl (C22:4)- phosphatidyl-ethanolamine (OOH-PE). The selenium-dependent glutathione peroxidase 4 (GPX4) inhibits ferroptosis, converting unstable ferroptotic lipid hydroperoxides to non-toxic lipid alcohols. The effect of GPX4 ablation is divergent among cells and tissues, suggesting that additional regulators may guard trophoblasts against ferroptosis. While placental oxidative stress and lipotoxicity are hallmarks of placental dysfunction, the possible role of ferroptosis in placental function has not been hitherto investigated. Here we found that placental dysfunction is associated with ferroptosis, and that inhibition of GPX4 causes trophoblast injury and ferroptosis in vitro and in vivo during mouse pregnancy. Importantly, we uncover a role for the phospholipase PLA2G6 (PNPLA9, iPLA2beta), known to metabolizes OOH-PE to lyso-PE and oxidized fatty acid, in mitigating ferroptosis induced by GPX4 inhibition in vitro or by hypoxia-reoxygenation injury in vivo. Together, we identified ferroptosis in the human and mouse placenta, and established a novel role for PLA2G6 in attenuating trophoblastic ferroptosis. Our data provide mechanistic insights to the ill-defined entity of placental lipotoxicity, and may inspire new therapeutic strategies that target PLA2G6 as a means to modulate ferroptosis in placental and non-placental tissue.

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Long noncoding RNA expression profiles in sub-lethal heat treated hepatoma carcinoma cells. (SMMC-7721 cells: sub-lethal heat treated vs. untreated)

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Legionella pneumophila cells after sub-lethal heat shock

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Sub-Lethal levels of Gentamicin impacts gonococcal gene expression

Project description:Sub-Lethal levels of Gentamicin impacts gonococcal gene expression

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Kristen-PAO1-anaerobic sub-lethal concentrations tobramycin

Project description:To see the effect of sub-lethal concentration of tobramcyin on PAO1 under anaerobic conditions. RNA was isolated from 5 biological repeats of PAO1 grown to mid-log phase in cationic adjusted mueller hinton broth containing 15mM KNO3 and 5 biological repeats of PAO1 grown to mid-log phase in cationic adjusted mueller hinton broth containing 15mM KNO3 and then treated for 30 minutes with 2 ug/ml tobramycin. All flasks were sealed to create anaerobic conditions. null

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Sub-Lethal levels of Gentamicin impacts gonococcal gene expression

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Adaptive Gene Profiling of Mycobacterium Tuberculosis during Sub-lethal Kanamycin Exposure

Project description:Objectives: Mtb adaptation is the major threat to affective disease control.The objective of this study was to identify major contributors participating in Mtb adaptation process during sub-lethal drug exposure through next generation sequencing Methods: The sequence reads that passed quality filters were analyzed through Tophat-2 and HT-Seq after being unified with housekeeping genes expression level.Adaptation analysis was performed through classifying genes expression in count table by K-Means clustering algorithm and find interested genes pattern Results: Genes responsible for lipid metabolism strongly repressed while involved in virulence and information pathways up regulated under sub-lethal kanamycin stress.Moreover an adaptive network comprise of Ra1750,Ra3160,Ra3161,Ra2492 and Ra3893 identified in kanamycin treated Mtb Conclusions: Mtb has a complex regulatory inter-connected gene network supporting its survival under diverse environmental conditions.

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