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Genome-wide maps of SMAD2-chromatin binding state in TGFbeta-treated vascular smooth muscle cells

ABSTRACT: Genome-wide maps of SMAD2-chromatin binding state in TGFbeta-treated vascular smooth muscle cells

PROVIDER: PRJNA445689 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6897992_1.fastq.gz	Fastqsanger.gz
	SRR6897992_2.fastq.gz	Fastqsanger.gz
	SRR6897993_1.fastq.gz	Fastqsanger.gz
	SRR6897993_2.fastq.gz	Fastqsanger.gz
	SRR6897994_1.fastq.gz	Fastqsanger.gz

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Genome-wide maps of SMAD2-chromatin binding state in TGFbeta-treated vascular smooth muscle cells

Project description:To further explore the role of these two factors in SMC reprogramming, we treated human aortic smooth muscle (HASMCs) in vitro with TGFβ and mapped binding of Smad2/3, which reflects TGFβ activity, and Pol2-Ser2p, which reflects transcriptional activity, by ChIP-seq analysis. Smad2/3 bound to numerous regulatory regions in the genome differentially regulating expression of numerous genes as demonstrate by alterations in Pol2-Serp2 binding profile and analysis of bulk RNA sequencing. Examination of the top 20 transcription factors identified by sequencing of Smad2/3 binding regulatory regions identified KLF4 gene as one of the most prominently regulated genes. Further analysis showed Smad2/3 binding to multiple KLF4 gene regulatory elements that increased following TGFβ treatment, indicating that KLF4 is a direct target of Smad2/3. At the same time, the amount of bound Pol2-Ser2p decreased, pointing to reduced transcriptional activity. In contrast, Smad2/3 did not bind to KLF2 or KLF5 regulatory elements, demonstrating that these genes are not directly regulated by TGFβ.

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