{"title":"Hydrogen Sulfide Ameliorates Homocysteine-Induced Mitochondrial Autophagy Disorder in HT22 Cells","authors":"Haijun Wei, Juan He, Xing Li, Mei Zhao, Fan Xiao","doi":"10.1134/s1819712424010252","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Damaged mitochondrial autophagy (mitophagy) caused by the elevated level of homocysteine (Hcy) or hyperhomocysteine (Hhcy) is closely related to neurodegenerative diseases. However, effective intervening strategies for Hcy-mediated impaired mitophagy have not been discovered. Hydrogen sulfide (H<sub>2</sub>S) act as a third gaseous modulator with neuroprotective and anti-oxidative properties. Here we hypothesized that the use of hydrogen sulfide in an in vitro model would ameliorate Hcy-induces mitotic dysfunction. The mouse hippocampal neuronal cell line (HT22) was pretreated with two concentrations (100, 200 μM) of NaHS before exposure to Hcy. The expression of autophagy related proteins, including Beclin-1, LC3-II, P62, was determined by western blotting. To evaluate mitochondrial function, mitochondrial membrane potential was monitored by flow cytometry after tetramethylrhodamine (TMRM) staining. The number of damaged mitochondria was also analyzed by flow cytometry after Mito-Tracker Red (MTR) staining. Our results demonstrated that Hcy caused significant down-regulation of Beclin-1, LC3-II, and up-regulation of P62, compared to normal cells (not pretreated with NaHS and not exposed to Hcy). However, hydrogen sulfide partially reversed the expression of the above three proteins in a dose-dependent manner. In addition, the Hcy-induced impaired mitochondrial membrane potential and impaired number were restored by pretreatment with NaHS. Taken together, hydrogen sulfide ameliorates Hcy-mediated mitochondrial phagocytic dysfunction and may serve as a potential interventional strategy to counteract the detrimental effects of Hcy on mitochondrial phagocytosis in neurodegenerative conditions.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":null,"pages":null},"PeriodicalIF":0.5000,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurochemical Journal","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1134/s1819712424010252","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Damaged mitochondrial autophagy (mitophagy) caused by the elevated level of homocysteine (Hcy) or hyperhomocysteine (Hhcy) is closely related to neurodegenerative diseases. However, effective intervening strategies for Hcy-mediated impaired mitophagy have not been discovered. Hydrogen sulfide (H2S) act as a third gaseous modulator with neuroprotective and anti-oxidative properties. Here we hypothesized that the use of hydrogen sulfide in an in vitro model would ameliorate Hcy-induces mitotic dysfunction. The mouse hippocampal neuronal cell line (HT22) was pretreated with two concentrations (100, 200 μM) of NaHS before exposure to Hcy. The expression of autophagy related proteins, including Beclin-1, LC3-II, P62, was determined by western blotting. To evaluate mitochondrial function, mitochondrial membrane potential was monitored by flow cytometry after tetramethylrhodamine (TMRM) staining. The number of damaged mitochondria was also analyzed by flow cytometry after Mito-Tracker Red (MTR) staining. Our results demonstrated that Hcy caused significant down-regulation of Beclin-1, LC3-II, and up-regulation of P62, compared to normal cells (not pretreated with NaHS and not exposed to Hcy). However, hydrogen sulfide partially reversed the expression of the above three proteins in a dose-dependent manner. In addition, the Hcy-induced impaired mitochondrial membrane potential and impaired number were restored by pretreatment with NaHS. Taken together, hydrogen sulfide ameliorates Hcy-mediated mitochondrial phagocytic dysfunction and may serve as a potential interventional strategy to counteract the detrimental effects of Hcy on mitochondrial phagocytosis in neurodegenerative conditions.
期刊介绍：
Neurochemical Journal (Neirokhimiya) provides a source for the communication of the latest findings in all areas of contemporary neurochemistry and other fields of relevance (including molecular biology, biochemistry, physiology, neuroimmunology, pharmacology) in an afford to expand our understanding of the functions of the nervous system. The journal presents papers on functional neurochemistry, nervous system receptors, neurotransmitters, myelin, chromaffin granules and other components of the nervous system, as well as neurophysiological and clinical aspects, behavioral reactions, etc. Relevant topics include structure and function of the nervous system proteins, neuropeptides, nucleic acids, nucleotides, lipids, and other biologically active components.
The journal is devoted to the rapid publication of regular papers containing the results of original research, reviews highlighting major developments in neurochemistry, short communications, new experimental studies that use neurochemical methodology, descriptions of new methods of value for neurochemistry, theoretical material suggesting novel principles and approaches to neurochemical problems, presentations of new hypotheses and significant findings, discussions, chronicles of congresses, meetings, and conferences with short presentations of the most sensational and timely reports, information on the activity of the Russian and International Neurochemical Societies, as well as advertisements of reagents and equipment.
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