Hui-ning HUANG, Juan-juan DU, Yi SUN, Ying-long HOU, Mei GAO. Proteomic analysis of left atrial appendage with atrial fibrillation induced by acute obstructive sleep apnea in rabbit models[J]. Chinese Heart Journal, 2021, 33(3): 244-250. DOI: 10.12125/j.chj.202103064
    Citation: Hui-ning HUANG, Juan-juan DU, Yi SUN, Ying-long HOU, Mei GAO. Proteomic analysis of left atrial appendage with atrial fibrillation induced by acute obstructive sleep apnea in rabbit models[J]. Chinese Heart Journal, 2021, 33(3): 244-250. DOI: 10.12125/j.chj.202103064

    Proteomic analysis of left atrial appendage with atrial fibrillation induced by acute obstructive sleep apnea in rabbit models

    •   AIM  To identify differentially expressed proteins in left atrial appendage of rabbits with acute obstructive sleep apnea (OSA)-induced atrial fibrillation by proteomic and explore the molecular biological mechanism.
        METHODS  Twelve rabbits were randomized into control group and OSA-induced atrial fibrillation group with 6 in each group. TMT relative quantitative technique was used to identify differentially expressed proteins and bioinformatics analysis was performed.
        RESULTS  According to the expression fold change of more than 1.2 times (up-regulation by more than 1.2 times or down-regulation by more than 0.83 times) and P<0.05, there were 54 proteins with statistical differences, of which 24 were up-regulated and 30 were down-regulated. Through bioinformatics analysis, it was found that binding, structural molecule activity, catalytic activity, molecular function regulator and transcription regulator activity were the main functions of differential proteins and they were mainly involved in important biological processes such as cellular process, biological process regulation, biological regulation, response to stimulus and metabolic process.
        CONCLUSION  The differential proteins identified may be related to the occurrence of acute OSA-induced atrial fibrillation, which provides a basis for further exploring the pathogenesis of atrial fibrillation induced by OSA.
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