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Klf2/4-independent effects of Pcdhg on gene expression in endothelial cells exposed to Oscillatory Shear Stress (OSS)

ABSTRACT: Klf2/4-independent effects of Pcdhg on gene expression in endothelial cells exposed to Oscillatory Shear Stress (OSS)

PROVIDER: PRJNA1134790 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29790450_1.fastq.gz	Fastqsanger.gz
	SRR29790450_2.fastq.gz	Fastqsanger.gz
	SRR29790451_1.fastq.gz	Fastqsanger.gz
	SRR29790451_2.fastq.gz	Fastqsanger.gz
	SRR29790452_1.fastq.gz	Fastqsanger.gz

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Klf2/4-independent effects of Pcdhg on gene expression in endothelial cells exposed to Oscillatory Shear Stress (OSS)

Project description:We found that Pcdhg is a potent suppressor of Klf2/4 in endothelial cells. We performed RNAseq analysis to characterize deregulated pathways and processes by which Pcdhg may regulate Klf2/4.

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KLF2-induced actin shear fibers control both alignment to flow and JNK signaling in vascular endothelium

Project description:The shear stress-induced transcription factor KrÃ¼ppel-like factor 2 (KLF2) confers anti-inflammatory properties to endothelial cells through inhibition of activator protein 1, presumably by interfering with MAPK cascades. To gain insight into the regulation of these cascades by KLF2, we used antibody arrays in combination with time-course mRNA micro-array analysis. No gross changes in MAPKs were detected, rather phosphorylation of actin cytoskeleton-associated proteins, including Focal Adhesion Kinase, was markedly repressed by KLF2. Furthermore, we demonstrate that KLF2-mediated inhibition of Jun NH2-terminal kinase (JNK) and its downstream targets ATF2/c-Jun is dependent on the cytoskeleton. Specifically, KLF2 directs the formation of typical short basal actin filaments, we term shear fibers, which are distinct from thrombin- or TNF-Î±-induced stress fibers. KLF2 is shown to be essential for shear stress-induced cell alignment, concomitant shear fiber assembly and inhibition of JNK signaling. These findings link the specific effects of shear-induced KLF2 on endothelial morphology to the suppression of JNK MAPK signaling in vascular homeostasis via novel actin shear fibers. Tramscriptome profiling: Three independent isolates of Human Umbilical Vein Endothelial cells were transduced with lentiviral vectors expressing Kruppel Like Factor 2 (KLF2) or no protein (mock), and at time after transduction 24 h, 48 h, 72 h , RNA was isolated and hybridized to GPL4868 microarrays using dye swap procedure Kinome profiling: Two independent isolates of Human Umbilical Vein Endothelial cells were transduced with lentiviral vectors expressing Kruppel Like Factor 2 (KLF2) or no protein (mock), and at time after transduction 72 h , total cellular protein was isolated and hybridized to Kinexus KAM-1.1 phosphoprotein (kinexus) microarrays using dual color procedure in duplicate

2010-06-25 | E-GEOD-19412 | biostudies-arrayexpress

KLF2-induced actin shear fibers control both alignment to flow and JNK signaling in vascular endothelium

Project description:The shear stress-induced transcription factor Krüppel-like factor 2 (KLF2) confers anti-inflammatory properties to endothelial cells through inhibition of activator protein 1, presumably by interfering with MAPK cascades. To gain insight into the regulation of these cascades by KLF2, we used antibody arrays in combination with time-course mRNA micro-array analysis. No gross changes in MAPKs were detected, rather phosphorylation of actin cytoskeleton-associated proteins, including Focal Adhesion Kinase, was markedly repressed by KLF2. Furthermore, we demonstrate that KLF2-mediated inhibition of Jun NH2-terminal kinase (JNK) and its downstream targets ATF2/c-Jun is dependent on the cytoskeleton. Specifically, KLF2 directs the formation of typical short basal actin filaments, we term shear fibers, which are distinct from thrombin- or TNF-α-induced stress fibers. KLF2 is shown to be essential for shear stress-induced cell alignment, concomitant shear fiber assembly and inhibition of JNK signaling. These findings link the specific effects of shear-induced KLF2 on endothelial morphology to the suppression of JNK MAPK signaling in vascular homeostasis via novel actin shear fibers.

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Expression profile of human lymphatic endothelial cells under static or oscillatory shear stress conditions in the presence or absence of FOXC2

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Shear stress-induced long non-coding RNA, NIMBUSS, is required for the KLF2-mediated gene expression profile associated with vascular homeostasis I

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Expression profile of human lymphatic endothelial cells under static or oscillatory shear stress conditions in the presence or absence of FOXC2

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