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Transcriptome-wide Profile of Cerebral Cavernous Malformations Patients Reveal Important Long noncoding RNA molecular signatures

ABSTRACT: Transcriptome-wide Profile of Cerebral Cavernous Malformations Patients Reveal Important Long noncoding RNA molecular signatures

PROVIDER: PRJNA565985 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10133336.fastq.gz	Fastqsanger.gz
	SRR10133337.fastq.gz	Fastqsanger.gz
	SRR10133338.fastq.gz	Fastqsanger.gz
	SRR10133339.fastq.gz	Fastqsanger.gz
	SRR10133340.fastq.gz	Fastqsanger.gz

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Systems Biology Proteomic Analysis of Cerebral Cavernous Malformation

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Project description:Cerebral cavernous malformations (CCMs) are anomalies that develop mainly in the cerebral vasculature. They result from mutations in CCM1/KRIT1, CCM2, or CCM3/PDCD10. Loss of CCM proteins triggers a MAPK-Krüppel-like factor 2 (KLF2) signaling cascade, which induces a pathophysiological pattern of gene expression within endothelial cells. The downstream target genes that are activated by KLF2 are mostly unknown. Here we show that Chromobox Protein Homolog 7 (CBX7), component of the Polycomb Repressive Complex 1, contributes to pathophysiological KLF2 signaling during zebrafish cardiovascular development. CBX7/cbx7a mRNA is strongly upregulated in lesions of CCM patients, and in human, mouse, and zebrafish CCM-deficient endothelial cells. The silencing or pharmacological inhibition of CBX7/Cbx7a suppresses pathological CCM phenotypes in ccm2 zebrafish, CCM2-deficient HUVECs, and in a pre-clinical murine CCM3 disease model. Whole-transcriptome datasets from zebrafish cardiovascular tissues and human endothelial cells reveal that CBX7/Cbx7a plays a role in the activation of KLF2 targets including genes encoding TEK, Angiopoietin1, WNT9, and endoMT proteins. Our findings uncover an intricate interplay in the regulation of Klf2-dependent biomechanical signaling by CBX7 in CCM. This work also provides insights for therapeutic strategies in the pathogenesis of CCM.

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