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RNAseq highlights the role of Sirt2 in protecting neuronal cell from cisplatin-treated injury

ABSTRACT: RNAseq highlights the role of Sirt2 in protecting neuronal cell from cisplatin-treated injury

PROVIDER: PRJEB36706 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3892740.fastq.gz	Fastqsanger.gz
	ERR3892750.fastq.gz	Fastqsanger.gz
	ERR3892741.fastq.gz	Fastqsanger.gz
	ERR3892751.fastq.gz	Fastqsanger.gz
	ERR3892742.fastq.gz	Fastqsanger.gz

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DNA repair drives cisplatin-induced neuronal death

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transcriptome analysis of SIRT2 dependent genes modulated during infection by Listeria monocytogenes

Project description:tissue culture cells were treated with an inhibitor to the deacetylase SIRT2 (AGK2) and infected with Listeria monocytogenes

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Metabolic control of adaptive b-cell proliferation by the protein deacetylase SIRT2

Project description:Selective and controlled expansion of endogenous b-cells has been pursued as a potential therapy for diabetes. Ideally, such therapies would preserve feedback control of b-cell proliferation to avoid excessive b-cell expansion and an increased risk of hypoglycemia. Here, we identified a regulator of b-cell proliferation whose inactivation results in controlled b-cell expansion: the protein deacetylase Sirtuin 2 (SIRT2). Sirt2 deletion in b-cells of mice increased b-cell proliferation during hyperglycemia with little effect in homeostatic conditions, indicating preservation of feedback control of b-cell mass. SIRT2 restrains proliferation of human islet b-cells cultured in glucose concentrations above the glycemic set point, demonstrating conserved SIRT2 function. Analysis of acetylated proteins in islets treated with a SIRT2 inhibitor revealed that SIRT2 deacetylates enzymes involved in oxidative phosphorylation, dampening the adaptive increase in oxygen consumption during hyperglycemia. At the transcriptomic level, Sirt2 inactivation has context-dependent effects on b-cells, with Sirt2 controlling how b-cells interpret hyperglycemia as a stress. Finally, we provide proof-of-principle that systemic administration of a GLP1-coupled Sirt2-targeting antisense oligonucleotide achieves b-cell selective Sirt2 inactivation and stimulates b-cell proliferation under hyperglycemic conditions. Overall, these studies identify a therapeutic strategy for increasing b-cell mass in diabetes without circumventing feedback control of b-cell proliferation.

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Sirt2-associated transcriptome modifications in cisplatin-induced neuronal injury.

Project description: Not available

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DNA repair drives cisplatin-induced neuronal death

Project description:Cisplatin and similar alkylating chemotherapy agents are the cornerstone treatments for many types of cancers. While effective, these drugs induce long-term side-effects in post-mitotic tissues including the nervous system. There are no known effective pharmacological interventions for chemotherapy-induced neurotoxicities, in part due to our limited understanding of how neurons and other non-dividing cells respond to DNA damage. Here, we show that nucleotide excision repair (NER) is responsible for cisplatin adduct removal in human neurons. However, contrary to its protective role in dividing cells, NER drives neuronal cell death in response to cisplatin. Through DNA repair synthesis, NER exhausts low levels of deoxynucleoside triphosphate (dNTP) pools found in post-mitotic neurons. dNTP pools are first consumed to resolve transcription blocking lesions through transcription-coupled NER. When dNTPs become exhausted, toxic double-strand breaks accumulate across the genome primarily because of incomplete global-genome NER. Supplementation with deoxynucleosides (dN) or genetic upregulation of dNTP production protects neurons from cisplatin-induced cell death. These results identify low levels of endogenous dNTP pools as a vulnerability of post-mitotic cells to DNA damage and suggest nucleoside supplementation as a strategy to protect patients from chemotherapy-induced neurotoxicity.

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DNA repair drives cisplatin-induced neuronal death [RNA-Seq]

Project description:DNA repair drives cisplatin-induced neuronal death [RNA-Seq]

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DNA repair drives cisplatin-induced neuronal death [END-seq]

Project description:DNA repair drives cisplatin-induced neuronal death [END-seq]

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DNA repair drives cisplatin-induced neuronal death [SAR-seq]

Project description:DNA repair drives cisplatin-induced neuronal death [SAR-seq]

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