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Transcriptome profiling of control cells or the A549 cells in the presence or absence of acetate following TGF-β1 stimulation

ABSTRACT: Transcriptome profiling of control cells or the A549 cells in the presence or absence of acetate following TGF-β1 stimulation

PROVIDER: PRJNA809029 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18090900_1.fastq.gz	Fastqsanger.gz
	SRR18090900_2.fastq.gz	Fastqsanger.gz
	SRR18090901_1.fastq.gz	Fastqsanger.gz
	SRR18090901_2.fastq.gz	Fastqsanger.gz
	SRR18090902_1.fastq.gz	Fastqsanger.gz

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Transcriptome profiling of control cells or the A549 cells in the presence or absence of acetate following TGF-β1 stimulation

Project description:Purpose: To compare the transcriptome profiling of control cells or the A549 cells in the presence or absence of acetate following TGF-β1 stimulation. Methods: A549 cells were treated with control, TGF-β1 or TGF-β1 plus acetate for 2 days. And then, we performed RNA sequencing for transcription profiling of control cells or the A549 cells in the presence or absence of acetate following TGF-β1 stimulation. The raw data were processed with bcl2fastq software and HISAT2. Results: From the transcriptome profiling and analysis, we got gene expression data of control group and in the presence or absence of acetate following TGF-β1 stimulation using A549 cells. Conclusion: The gene expression data revealed the transcriptome variation by TGF-β1 treatment and acetate can reverse TGF-β1 effect.

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Project description:These data show that the genes that distinguish myofibroblasts from fibroblasts are myriad, and that some genes not traditionally associated with myofibroblast differentiation may serve as novel therapeutic targets for fibrosing disorders. Gene expression levels were assessed from total RNA on the Affymetrix U219 microarray. Here, we use transforming growth factor-β1 (TGF-β1) and prostaglandin E2 (PGE2), which has recently been shown to reverse myofibroblast differentiation, to investigate the transcriptomic changes that occur during TGF-β1-induced differentiation and PGE2-induced de-differentiation of myofibroblasts.

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