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The Role of FOXO4/NFAT2 Signaling Pathway in Dysfunction of Human Coronary Endothelial Cells and Inflammatory Infiltration of Vasculitis in Kawasaki Disease

ABSTRACT: The Role of FOXO4/NFAT2 Signaling Pathway in Dysfunction of Human Coronary Endothelial Cells and Inflammatory Infiltration of Vasculitis in Kawasaki Disease

PROVIDER: PRJNA863646 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20715415_1.fastq.gz	Fastqsanger.gz
	SRR20715415_2.fastq.gz	Fastqsanger.gz
	SRR20715416_1.fastq.gz	Fastqsanger.gz
	SRR20715416_2.fastq.gz	Fastqsanger.gz
	SRR20715417_1.fastq.gz	Fastqsanger.gz

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The Role of FOXO4/NFAT2 Signaling Pathway in Dysfunction of Human Coronary Endothelial Cells and Inflammatory Infiltration of Vasculitis in Kawasaki Disease

Project description:Aims: The Ca+/NFAT (Nuclear factor of activated T cells) signaling pathway activation is implicated in the pathogenesis of Kawasaki disease (KD); however, we lack detailed information regarding the regulatory network involved in the human coronary endothelial cell dysfunction and cardiovascular lesion development. Herein, we aimed to use mouse and endothelial cell models of KD vasculitis in vivo and in vitro to characterize the regulatory network of NFAT pathway in KD. Methods and Results: Among the NFAT gene family, NFAT2 showed the strongest transcriptional activity in peripheral blood mononuclear cells (PBMCs) from patients with KD. Then, NFAT2 overexpression and knockdown experiments in Human coronary artery endothelial cells (HCAECs) indicated that NFAT2 overexpression disrupted endothelial cell homeostasis by regulation of adherens junctions, whereas its knockdown protected HCAECs such dysfunction. Combined analysis using RNA sequencing and transcription factor (TF) binding site analysis in the NFAT2 promoter region predicted regulation by Forkhead box O4 (FOXO4). Western blotting, chromatin immunoprecipitation, and luciferase assays validated that FOXO4 binds to the promoter and transcriptionally represses NFAT2. Moreover, Foxo4 knockout increased the extent of inflamed vascular tissues in a mouse model of KD vasculitis. Functional experiments showed that inhibition NFAT2 relieved Foxo4 knockout exaggerated vasculitis in vivo.

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Project description:AKT1 is a serine/threonine kinase implicated in fetal, placental, and postnatal growth. In this study, we investigated roles for AKT1 in placental development using a genome-edited/loss-of-function rat model. Both heterozygous and homozygous Akt1 mutant rats were viable and fertile. Disruption of AKT1 resulted in placental, fetal, and postnatal growth restriction. Akt1 null placentas showed deficits in both junctional zone and labyrinth zone size and their ability to adapt to a physiological stressor. Robust differences in the transcriptome of wild type versus Akt1 null junctional zones were identified. Among the differentially expressed junctional zone transcripts was forkhead box O4 (Foxo4), which encodes a transcription factor and known AKT substrate. FOXO4 expression was prominent in the junctional zone and invasive trophoblast cells of the rat placentation site and enhanced following rat TS cell differentiation. Foxo4 gene disruption using genome-editing resulted in placentomegaly, including an enlarged junctional zone. AKT1 and FOXO4 regulate the expression of many of the same transcripts expressed by trophoblast cells; however, in opposite directions. In summary, we have identified AKT1 and FOXO4 as part of a regulatory network controlling hemochorial placenta development.

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