DOI: 10.57760/sciencedb.j00217.04037
title: The Relationship between mitochondrial levels in coronary artery endothelial cells and activation of nuclear factor in activated T cells in a mouse model of immune vasculitis.
title: 小鼠免疫性血管炎模型中冠状动脉内皮细胞线粒体与活化T细胞核因子水平表达的关系

description: Objective Exploration of the correlation between mitochondrial lesions in coronary artery endothelial cells and nuclear factor of activated T cells(NFAT)in the immune vasculitis model of Kawasaki disease in mice.Methods Using white Candida fragment water-soluble polysaccharide fraction(CAWS)to induce Kawasaki disease immune vasculitis animal model in C57/BL6 mice,electron microscopy was used to observe mitochondrial pathological changes in coronary artery endothelial cells;Real-time PCR was used to measure the expression levels of NFAT1 and NFAT2mRNA in peripheral blood mononuclear cells of mice.Results Transmission electron microscopy results showed that in the experimental group during the acute phase(3 days),mitochondria exhibited significant swelling,accompanied by vacuole formation and matrix loosening, with internal structure loss.Subacute phase(17 days)mitochondrial swelling is reduced compared to the acute phase.In the recovery phase(24 days),mitochondrial swelling was reduced,internal cristae were visible,and some structures returned to normal.Real-time PCR results revealed that compared to the control group,during the initial 3 days of the experiment,the mRNA expression levels of NFAT1 and NFAT2 in the experimental group were notably elevated compared to the control group(P&lt;0.05).In the subsequent 17 days,the mRNA expression levels of NFAT1 and NFAT2 remained significantly higher in the experimental group compared to the control group(P&lt;0.05).However,by day 24 during the recovery phase,the mRNA expression levels of NFAT1 and NFAT2 had significantly decreased and were no longer significantly different from those in the control group(P&gt;0.05).Conclusions In the mouse model of Kawasaki disease immunoglobulin vasculitis,mitochondria and NFAT1、NFAT2 show synchronicity in the pathological changes and molecular expression at different stages of inflammation,indicating their correlation and relevance to the development of Kawasaki disease.
description: Objective Exploration of the correlation between mitochondrial lesions in coronary artery endothelial cells and nuclear factor of activated T cells(NFAT)in the immune vasculitis model of Kawasaki disease in mice.Methods Using white Candida fragment water-soluble polysaccharide fraction(CAWS)to induce Kawasaki disease immune vasculitis animal model in C57/BL6 mice,electron microscopy was used to observe mitochondrial pathological changes in coronary artery endothelial cells;Real-time PCR was used to measure the expression levels of NFAT1 and NFAT2mRNA in peripheral blood mononuclear cells of mice.Results Transmission electron microscopy results showed that in the experimental group during the acute phase(3 days),mitochondria exhibited significant swelling,accompanied by vacuole formation and matrix loosening, with internal structure loss.Subacute phase(17 days)mitochondrial swelling is reduced compared to the acute phase.In the recovery phase(24 days),mitochondrial swelling was reduced,internal cristae were visible,and some structures returned to normal.Real-time PCR results revealed that compared to the control group,during the initial 3 days of the experiment,the mRNA expression levels of NFAT1 and NFAT2 in the experimental group were notably elevated compared to the control group(P&lt;0.05).In the subsequent 17 days,the mRNA expression levels of NFAT1 and NFAT2 remained significantly higher in the experimental group compared to the control group(P&lt;0.05).However,by day 24 during the recovery phase,the mRNA expression levels of NFAT1 and NFAT2 had significantly decreased and were no longer significantly different from those in the control group(P&gt;0.05).Conclusions In the mouse model of Kawasaki disease immunoglobulin vasculitis,mitochondria and NFAT1、NFAT2 show synchronicity in the pathological changes and molecular expression at different stages of inflammation,indicating their correlation and relevance to the development of Kawasaki disease.