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Single-cell RNAseq (10x Genomics) analysis of the abdominal aorta in a murine model of Kawasaki disease vasculitis

ABSTRACT: Single-cell RNAseq (10x Genomics) analysis of the abdominal aorta in a murine model of Kawasaki Disease vasculitis (Lactobacillus casei cell wall extract, LCWE) and in control PBS-injected mice

ORGANISM(S): Mus musculus

PROVIDER: GSE178765 | GEO | 2021/09/14

REPOSITORIES: GEO

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Single-cell RNAseq (10x Genomics) analysis of the abdominal aorta in a murine model of Kawasaki disease vasculitis

Project description:Single-cell RNAseq (10x Genomics) analysis of the abdominal aorta in a murine model of Kawasaki disease vasculitis

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Spatial transcriptomics (Visium, Spatial 3' V1, 10x Genomics) analysis of heart tissues in a murine model of Kawasaki disease vasculitis

Project description:Spatial transcriptomics (Visium, Spatial 3' V1, 10x Genomics) analysis of heart tissues from Lactobacillus casei cell wall extract (LCWE)-injected mice and control PBS-injected mice

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Sex differences in LCWE-induced model of Kawasaki Disease vascultitis and response to Anakinra treatment

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Proteomics - LCWE Kawasaki Model

Project description:Murine vasculitis was induced via Lactobacillus casei cell wall extract (LCWE) injection in 5-week-old male mice. Groups of mice were injected with LCWE alone, LCWE and the IL-1 receptor antagonist anakinra, or saline for controls. Upper heart tissue was assessed by quantitative mass spectrometry analysis.

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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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Expression data from the abdominal aorta and abdominal aortic aneurysm

Project description:Global gene expression information that can be used to identify pathways involved in the pathophysiology of disease. We used microarrays to identify which genes are expressed in either the abdominal aorta (control) or in abdominal aortic aneurysms (case), and also which genes may be differential between the two tissue states. Keywords: Characterization of expression in both diseased and non-diseased abdominal aortas.

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RNA-sequencing of abdominal aortic aneurysm (AAA) and control abdominal aorta tissues

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MCM8 mediated mitophagy protects vascular health in response to nitric oxide signaling in a mouse model of Kawasaki disease

Project description:Mitophagy is a major quality control pathway that removes unwanted or dysfunctional mitochondria, and plays an essential role in vascular health. Here we show that MCM8 expression is significantly decreased in children with Kawasaki disease (KD) who developed coronary artery aneurysms. Mechanistically, we discover that nitric oxide (NO) signaling promotes TRIM21 mediated MCM8 ubiquitination, which disrupts its interaction with MCM9 and promotes its cytosolic export. In the cytosol, MCM8 relocates to the mitochondria pore forming proteins and promotes their ubiquitination by TRIM21. In addition, MCM8 directly recruits LC3 via its LIR motif and initiates mitophagy. This suppresses mitochondrial DNA-mediated activation of type I interferon via cGAS and STING. Mice that are deficient in Mcm8, Trim21, Nos2, or reconstituted with the East-Asian specific MCM8-P276 variant develop more severe coronary artery vasculopathy in the Lactobacillus casei extract-induced KD model. Collectively, the data suggest that MCM8 protects vascular health in the KD setting.

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