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Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling [ChIP-Seq]

ABSTRACT: Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling [ChIP-Seq]

PROVIDER: PRJNA1211995 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32032896_1.fastq.gz	Fastqsanger.gz
	SRR32032896_2.fastq.gz	Fastqsanger.gz
	SRR32032897_1.fastq.gz	Fastqsanger.gz
	SRR32032897_2.fastq.gz	Fastqsanger.gz
	SRR32032898_1.fastq.gz	Fastqsanger.gz

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Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling

Project description:Angiogenesis is a dynamic process fine-tuned by transcription factors in endothelial cells. The Krüpple-like factor 15 (KLF15)-mediated transcriptional regulation mechanism is critical for cardiovascular diseases. However, the role of endothelial KLF15 in governing angiogenesis remains unknown.KLF15 and vasorin (VASN) were deleted from endothelial cells using tamoxifen-inducible Cdh5-promoter-driven Cre recombinase in EC-KLF15 KO and EC-VASN KO mice, respectively. EC-KLF15 KO, EC-VASN KO and control mice were subjected to retinal angiogenesis or tumor cell transplantation. The RNA sequencing (RNA-seq), ATAC-seq, and ChIP-seq were conducted to identify VASN as a downstream effector of KLF15. Cell proliferation, wound healing, tube formation, and sprouting assays were performed to delineate endothelial cell function. In EC-KLF15 KO mice and adenovirus-mediated KLF15 overexpression mice, we showed that KLF15 negatively regulated retinal angiogenesis, as confirmed in cultured endothelial cells. KLF15 opened chromatin, bound to the promoters of GC-rich sequences, and transactivated the expression of VASN. Subsequently, VASN suppressed endothelial angiogenic function which was essential for Dll4-induced Notch1 signaling activation. Moreover, increased expression of VASN in EC-KLF15 KO mice suppressed retinal angiogenesis, which was attenuated by γ-secretase inhibitor. EC-VASN KO mice recapitulated the promotion of retinal angiogenesis in EC-KLF15 KO mice. Finally, the EGF-like domain of VASN was essential for its interaction with Notch1, and VASN EGF-like domain-derived peptides activated Notch1 signaling and suppressed angiogenesis.The KLF15/VASN axis negatively regulates angiogenesis by activating Notch1 signaling. KLF15 and VASN in endothelial cells might represent novel therapeutic targets for the treatment of impaired angiogenesis-related diseases and tumors.

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Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling

Project description:Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling

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Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling [ATAC-Seq]

Project description:Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling [ATAC-Seq]

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Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling [ChIP-Seq]

Project description:Kruppel like factors (KLFs) are a subfamily of zinc finger proteins. As one of the family members, KLF15 can specifically bind to GC rich sequences on the promoter, thereby exerting transcriptional regulatory effects. Here we found that KLF15 negatively regulates angiogenesis in endothelial cells. KLF15 induces an increase in vasorin (VASN) expression, thereby activating the Notch signaling pathway and leading to a decrease in angiogenesis. These findings point to an KLF15/VASN axis as critical determinants of Notch signaling activation.

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Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling [ATAC-Seq]

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