过氧化物酶体生物发生因子5控制组蛋白去乙酰化酶6和情景蛋白1的表达,调节大鼠海马背侧线粒体生物发生

IF 0.3 Q4 PHYSIOLOGY Physiology and Pharmacology Pub Date : 2021-12-01 DOI:10.52547/phypha.25.4.10
Shahrbanoo Rafiei, F. Khodagholi, F. Motamedi, L. Dargahi
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引用次数: 0

摘要

线粒体和过氧化物酶体是紧密相连的细胞器,在脂质氧化和氧化还原稳态的维持中相互合作。然而,过氧化物酶体在线粒体调节因子的调节中的作用仍未得到解答。SIRT1PGC-1α相互作用是能量消耗导致线粒体生物发生的关键途径。组蛋白去乙酰化酶(HDAC)6和HDAC10也调节线粒体动力学。线粒体功能障碍是衰老和神经退行性疾病的原因和/或后果。方法:在本研究中,通过慢病毒介导的shRNA,在海马背侧下调PEX5,以干扰蛋白质进入过氧化物酶体。通过评估过氧化氢酶活性、常规过氧化物酶基质酶以及PMP70和PEX14的表达,探讨了PEX5减少对过氧化物酶体的影响。然后,采用定量聚合酶链反应检测线粒体生物发生因子、PGC-1α和线粒体转录因子A (TFAM),采用western blotting检测线粒体相关hdac、SIRT1、SIRT3、HDAC6和HDAC10。此外,采用Morris水迷宫任务评估空间学习和记忆能力。结果:我们的研究结果显示,HDAC6和SIRT1显著降低,线粒体生物发生因子PGC-1α和TFAM降低,HDAC10和SIRT3无变化。尽管观察到这些变化,实验组的记忆表现并没有明显的变化。这些数据表明过氧化物酶体通过调控HDAC6和SIRT1的表达来调节线粒体动力学。结论:过氧化物酶体功能障碍可能发生在线粒体衰竭的上游,可以被认为是衰老和年龄相关疾病的潜在治疗靶点。
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Peroxisome biogenesis factor 5 controlled Histone deacetylase 6 and Situin1 expression and modulatedmitochondrial biogenesis in rat dorsal hippocampus
Introduction: Mitochondria and peroxisomes are tightly connected organelles that cooperate in lipid oxidation and maintenance of redox homeostasis. However, the peroxisome’s role in the modulation of the mitochondrial regulatory factors has remained unanswered. SIRT1PGC-1α interaction as a pivotal pathway in energy expenditure leads to mitochondrial biogenesis. Histone deacetylase (HDAC)6 and HDAC10 also regulate mitochondrial dynamics. Mitochondrial dysfunction is a cause and/or consequence of aging and neurodegenerative disorders. Methods: In this study, to disturb importing proteins into the peroxisomes, PEX5 was down-regulated in the dorsal hippocampus by lentivirus-mediated shRNA. The impact of PEX5 reduction on peroxisomes was explored by assessment of catalase activity, a regular peroxisome matrix enzyme, and PMP70 and PEX14 expression. Then, mitochondrial biogenesis factors, PGC-1α, and mitochondrial transcription factor A (TFAM) were measured by quantitative polymerase chain reaction and mitochondrial-related HDACs, SIRT1, SIRT3, HDAC6 and HDAC10, by western blotting. Besides, spatial learning and memory were assessed using the Morris water maze task. Results: Our results revealed a significant reduction of HDAC6 and SIRT1, alongside with decrease in mitochondrial biogenesis factors PGC-1α and TFAM, and no alteration in HDAC10 and SIRT3. Despite all observed changes, memory performance displayed no detectable alteration in the experimental groups. These data suggest the role of peroxisomes in modulating mitochondrial dynamics via regulation of HDAC6 and SIRT1 expression. Conclusion: Peroxisome dysfunctions may occur upstream to mitochondrial failure and can be considered as a potential therapeutic target for aging and age-related disorders.
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期刊介绍: Physiology and Pharmacology is the official English publication of the Iranian Society of Physiology and Pharmacology. The journal publishes Review articles, Full-length original articles, Letter to editor and Short communications in physiology, pharmacology and related subjects. The aim of this journal is to provide a medium of scientific communication for investigators in the field of Physiology and Pharmacology. The editors will welcome original basic and applied research articles from Physiologists and Pharmacologists. Articles should be in English language. The papers submitted to this journal must not be Published or under consideration for publication elsewhere. Physiology and Pharmacology is an open access journal which means that all contents is freely available without charge to the user or his/her institution. Users are allowed to read, download, copy, distribute, print, search or link to the full text of the articles in this journal without asking prior permission from the publisher or the author.
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