The association between oxidative stress and endothelial dysfunction in early childhood patients with Kawasaki disease

Ishikawa, Takamichi; Seki, Keigo

doi:10.1186/s12872-018-0765-9

Cited by 33 publications

(33 citation statements)

References 30 publications

(33 reference statements)

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“…Oxidative stress serves a key function in the pathophysiology of diseases including hypertension and AS by causing endothelial dysfunction (3). Clinical studies have identified that risk factors leading to AS exert adverse effects on the number and function of endothe-lial progenitor cells, limiting the capability for angiogenesis in patients (4). Oxidative stress has been identified to be associated with the pathogenesis of AS (4).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-140-5p aggravates hypertension and oxidative stress of atherosclerosis via targeting Nrf2 and Sirt2

et al. 2018

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In the present study, the function of microRNA (miR)-140-5p on oxidative stress in mice with atherosclerosis was investigated. A reverse transcription-quantitative polymerase chain reaction assay was used to determine the expression of miR-140-5p. Oxidative stress kits and reactive oxygen species (ROS) kits were used to analyze alterations in oxidative stress and ROS levels. The alterations in protein expression were determined using western blot analysis and an immunofluorescence assay. miR-140-5p expression was increased in mice with atherosclerosis with hypertension. Consistently, miR-140-5p expression was also increased in mice with atherosclerosis. Upregulation of miR-140-5p increased oxidative stress and ROS levels by suppressing the protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2), sirtuin 2 (Sirt2), Kelch-like enoyl-CoA hydratase-associated protein 1 (Keap1) and heme oxygenase 1 (HO-1) in vitro. By contrast, downregulation of miR-140-5p decreased oxidative stress and ROS levels by activating the protein expression of Nrf2, Sirt2, Keap1 and HO-1 in vitro. Sirt2 agonist or Nrf2 agonist inhibited the effects of miR-140-5p on oxidative stress in vitro. Collectively, these results suggested that miR-140-5p aggravated hypertension and oxidative stress of mice with atherosclerosis by targeting Nrf2 and Sirt2.

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Section: Introductionmentioning

confidence: 99%

“…Clinical studies have identified that risk factors leading to AS exert adverse effects on the number and function of endothe-lial progenitor cells, limiting the capability for angiogenesis in patients (4). Oxidative stress has been identified to be associated with the pathogenesis of AS (4).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-140-5p aggravates hypertension and oxidative stress of atherosclerosis via targeting Nrf2 and Sirt2

et al. 2018

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“…Table 2 demonstrated that seven of the ten most significant GO items were inflammation, immune or stress-related functions, which was consistent with the fact that KD is an acute inflammatory disease. In addition, KD was also characterized with oxidative stress 26,27 . Therefore, iTRAQ gel-free proteomics resulted in a reliable dataset deserving further investigations.…”

Section: Resultsmentioning

confidence: 99%

Serum proteins may facilitate the identification of Kawasaki disease and promote in vitro neutrophil infiltration

Huang

Weng

et al. 2020

Sci Rep

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Kawasaki disease (KD) usually affects the children younger than 5 years of age and subsequently causes coronary artery lesions (CALs) without timely identification and treatment. Developing a robust and fast prediction method may facilitate the timely diagnosis of KD, significantly reducing the risk of CALs in KD patients. The levels of inflammatory serum proteins dramatically vary during the onsets of many immune diseases, including in KD. However, our understanding of their pathogenic roles in KD is behind satisfaction. The purpose of this study was to evaluate candidate diagnostic serum proteins and the potential mechanism in KD using iTRAQ gel-free proteomics. We enrolled subjects and conducted iTRAQ gel-free proteomics to globally screen serum proteins followed by specific validation with ELISA. Further in vitro leukocyte trans-endothelial model was also applied to investigate the pathogenesis roles of inflammatory serum proteins. We identified six KD protein biomarkers, including Protein S100-A8 (S100A8), Protein S100-A9 (S100A9), Protein S100-A12 (S100A12), Peroxiredoxin-2 (PRDX2), Neutrophil defensin 1 (DEFA1) and Alpha-1-acid glycoprotein 1 (ORM1). They enabled us to develop a high-performance KD prediction model with an auROC value of 0.94, facilitating the timely identification of KD. Further assays concluded that recombinant S100A12 protein treatment activated neutrophil surface adhesion molecules responsible for adhesion to endothelial cells. Therefore, S100A12 promoted both freshly clinically isolated neutrophils and neutrophil-like cells to infiltrate through the endothelial layer in vitro. Finally, the antibody against S100A12 may attenuate the infiltration promoted by S100A12. Our result demonstrated that evaluating S100A8, S100A9, S100A12, PRDX2, DEFA1 and ORM1 levels may be a good diagnostic tool of KD. Further in vitro study implied that S100A12 could be a potential therapeutic target for KD.

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“…There is an increasing body of evidence that KD involves widespread endothelial dysfunction, such endothelial dysfunction might be induced by reactive oxygen species. It endothelial dysfunction and inflammation in patients with KD is not limited to coronary endothelium but involves renal and mesenteric vascular endothelium and might persist long after resolution of KD [30,31].…”

Section: Endothelial Inflammation In Both Disordersmentioning

confidence: 99%

Unleashing the mysterious link between COVID-19 and a famous childhood vasculitis: Kawasaki disease

AbdelMassih

AbdelAzeam

Ayad

et al. 2020

Egypt Pediatric Association Gaz

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Background: Coronavirus disease 2019 (COVID-19) emerged as a small outbreak in Wuhan rapidly progressing into the deadliest pandemic since the Spanish flu of 1918. The disease was deemed trivial in children, until the reporting, few days ago, of an emerging pediatric multi-inflammatory syndrome mimicking Kawasaki disease (KD). Main body: This report reveals that coronaviridae were implicated in induction of several post-infectious vasculitides, namely, KD, AHEI, and HSP. This occurs in genetically susceptible individuals to vascular inflammation. Shared genetic susceptibilities between KD and CoV include genes encoding for CD 40, HLAB-15:03, and ACE. This leads to augmented inflammation with hypersecretion of cytokines especially IL-6. Conclusion: The revealed relationships between KD and CoV can help to predict the risk of KD in COVID-19 patients through screening levels of upregulated cytokines. It might also signify that classic treatment of KD with IVIG might need to be replaced with anti-cytokine therapy in COVID-19 patients.

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The association between oxidative stress and endothelial dysfunction in early childhood patients with Kawasaki disease

Cited by 33 publications

References 30 publications

MicroRNA-140-5p aggravates hypertension and oxidative stress of atherosclerosis via targeting Nrf2 and Sirt2

MicroRNA-140-5p aggravates hypertension and oxidative stress of atherosclerosis via targeting Nrf2 and Sirt2

Serum proteins may facilitate the identification of Kawasaki disease and promote in vitro neutrophil infiltration

Unleashing the mysterious link between COVID-19 and a famous childhood vasculitis: Kawasaki disease

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