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Danio rerio

ABSTRACT: Tris(1,3-dichloro-2-propyl) phosphate Exposure During Early-Blastula Alters the Normal Trajectory of Zebrafish Embryogenesis

PROVIDER: PRJNA475635 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7789520.fastq.gz	Fastqsanger.gz
	SRR7789530.fastq.gz	Fastqsanger.gz
	SRR7789540.fastq.gz	Fastqsanger.gz
	SRR7789550.fastq.gz	Fastqsanger.gz
	SRR7789560.fastq.gz	Fastqsanger.gz

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Expression data from HeLa cell treated with Tris(1,3-dichloro-2-propyl)phosphate

Project description:Tris(1,3-dichloro-2-propyl)phosphate is widely used in consumer products as a flame retardant. Humans are often exposed to this compound. However, the molecular mechanisms of the compound`s adverse effects are still unclear. We address the molecular and cellular mechanisms underlying tris(1,3-dichloro-2-propyl)phosphate effects on HeLa cells. Here RNA-Seq analysis was performed to identify distinct classes of up- or down-regulated genes and their connections to different metabolic pathways.

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Project description:Human cell cultures A549 and HepG2/C3 were exposed to 0-100 micromolar Tris(1,3-dichloro-2-propyl)phosphate (TDCIPP) in 0.5% DMSO or to 0.5% DMSO alone for 24 h. RNA was prepared and labeled with Cy3. Agilent SurePrint G3 Human GE v2 8x60k Microarrays, Agilent design ID 039494, were used to profile transcriptional responses to TDCIPP.

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Expression data from HeLa cell treated with Tris(1,3-dichloro-2-propyl)phosphate

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Lysosome-autophagy dysfunction contribute to TDCIPP induced Aβ1-42 production in N2a-APPswe cells.

Project description:Alzheimer's disease is the most common form of dementia characterized on cognitive impairment. Autophagy-lysosome dysfunction is linked to AD pathology. Tris (1,3-dichloro-2-propyl) phosphate (TDCIPP) is a widely used organophosphorus flame retardants with the potential to induce neuronal damage. We found that TDCIPP significantly increased expression of BACE1 and of Aβ42. TMT labeled proteomic study were used to reveal profile changes of N2a-APPswe cells after exposure by TDCIPP. Proteomic and bioinformatic analysis revealed that lysosomal proteins were dysregulated after TDCIPP treatment in N2a-APPswe cells. LC3, P62, CTSD, and LAMP1 were increased, while STAT1 was decreased after TDCIPP exposure and dysregulated proteins were validated by Western blotting. Our results, for the first time revealed that TDCIPP could be one of potential environment risk factors for AD development. Autophagy dysregulation may take an important role on TDCIPP induced Aβ42 production.

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