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Pseudogenization of the humanin gene is common in the mitochondrial DNA of many vertebrates

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Zoological Research 2017年第4期38卷 198-202页

作者： lan S. Logan 22 Parkside Drive Exmouth Devon UK

In the human the peptide humanin is produced from the small humanin gene which is embedded as a gene-within-a-gene in the 16S ribosomal molecule of the mitochondrial DNA （mtDNA）. The peptide itself appears to be significant in the prevention of cell death in many tissues and improve cognition in animal models. By using simple data mining techniques, it is possible to show that 99.4% of the human humanin sequences in the GenBank database are unaffected by mutations. However, in other vertebrates, pseudogenization of the humanin gene is a common feature; occurring apparently randomly in some species and not others. The persistence, or loss, of a functional humanin gene may be an important factor in laboratory animals, especially if they are being used as animal models in studies of Alzheimer＇s disease （AD）. The exact reason why humanin underwent pseudogenization in some vertebrate species during their evolution remains to be determined. This study was originally planned to review the available information about humanin and it was a surprise to be able to show that pseudogenization has occurred in a gene in the mtDNA and is not restricted solely to chromosomal genes.

关键词： mtDNA humanin Pseudogenization NUMT

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Current Medical Science 2023年第3期43卷 579-584页

作者： Yi XIA Han-yong ZHANG Sha MA Fang ZHOU The Second Clinical Medical College Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China School of Stomatology Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Reproductive Center Wuhan Children's Hospital(Wuhan Maternal and Child Healthcare Hospital)Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430015China Department of Reproductive Medicine Maternal and Child Health Hospital of Hubei ProvinceTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430070China

Objective This study examined humanin expression in rat ovarian tissue,its cellular localization,and its correlation with rat age under physiological *** A total of 40 Sprague-Dawley rats of various ages(2,12,30,and 60 days old and 1 year old)were grouped by *** and immunohistochemical techniques were used to observe humanin expression and cellular location in the ovarian tissues of rats from each age *** addition,Western blotting and Real-time quantitative reverse transcription PCR(qRT-PCR)techniques were used to measure humanin expression level in the ovarian tissues of rats from each age *** The immunofluorescence and immunohistochemical results confirmed that humanin was expressed in rat ovarian *** addition,cellular localization analysis showed that humanin was expressed in the cytoplasm of oocytes,interstitial cells,granulosa cells and theca cells in all levels of follicles after the primary follicles,and in the corpus *** qRT-PCR results revealed that the level of humanin expression in the ovarian tissues of 12-day-old rats was non-significantly higher than that in the ovarian tissues of 2-day-old rats(P>0.05),whereas the levels of humanin expression in the ovarian tissues of 30-day-old,60-day-old,and 1-year-old rats were significantly lower than that in the ovarian tissues of 2-day-old rats(Phumanin protein expression in the ovarian tissues of 60-day-old and 1-year-old rats were significantly lower than those of 2-day-old rats(Phumanin protein expression between the ovarian tissues of 12-day-old and 30-day-old *** This study confirmed that humanin is expressed in the cytoplasm of various cells in rat ovarian ***,the level of humanin expression was highest in the ovarian tissues of 12-day-old rats,and it subsequently decreased with ***

关键词： humanin ovarian aging rat female fertility

humanin attenuates Alzheimer-like cognitive deficits and pathological changes induced by amyloid β-peptide in rats

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Neuroscience Bulletin 2014年第6期30卷 923-935页

作者： Gao-Shang Chai Dong-Xiao Duan Rong-Hong Ma Jian-Ying Shen Hong-Lian Li Zhi-Wei Ma Yu Luo Lu Wang Xin-Hua Qi Qun Wang Jian-Zhi Wang Zelan Wei Darrell D.Mousseau Li Wang Gongping Liu Department of Pathophysiology Key Laboratory of Neurological Diseases of Chinese Ministry of EducationTongji Medical CollegeHuazhong University of Science and Technology Department of Basic Medical Wuxi Medical SchoolJiangnan University Department of Physiology Basic Medical CollegeZhengzhou University Department of Laboratory Medicine Union HospitalHuazhong University of Science and Technology Department of Histology and Embryology Tongji Medical CollegeHuazhong University of Science and Technology Affiliated Hospital of Hebei University of Engineering Department of Psychiatry College of MedicineUniversity of SaskatchewanSaskatoonSaskatchewanS7N 5E5Canada Department of Pathophysiology Henan Medical College

Amyloid β-peptide（Aβ） has been implicated as a key molecule in the neurodegenerative cascades of Alzheimer ’s disease（AD）. humanin（HN） is a secretory peptide that inhibits the neurotoxicity of Aβ. However, the mechanism（s） by which HN exerts its neuroprotection against Aβ-induced ADlike pathological changes and memory deficits are yet to be completely defined. In the present study,we provided evidence that treatment of rats with HN increases the number of dendritic branches and the density of dendritic spines, and upregulates pre- and post-synaptic protein levels; these effects lead to enhanced long-term potentiation and amelioration of the memory deficits induced by Aβ1-42. HN also attenuated Aβ1-42-induced tau hyperphosphorylation,apparently by inhibiting the phosphorylation of Tyr307 on the inhibitory protein phosphatase-2A（PP2A）catalytic subunit and thereby activating PP2 A. HN also inhibited apoptosis and reduced the oxidativestress induced by Aβ1-42. These findings provide novel mechanisms of action for the ability of HN to protect against Aβ1-42-induced AD-like pathological changes and memory deficits.

关键词： humanin amyloid-beta Alzheimer’s disease tau apoptosis

humanin对鱼藤酮诱导的多巴胺神经元毒性的保护作用研究

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陆军军医大学学报 2024年第7期46卷 670-677页

作者：单耀辉张启夫程晋叶枫张玺余文珮王晓刚赵远鹏但国蓉陈明亮赛燕陆军军医大学(第三军医大学)军事预防医学系防化医学教研室重庆400038

目的探讨humanin(HN)对鱼藤酮(rotenone,Rot)诱导的多巴胺神经元毒性损伤的保护作用和机制。方法构建Rot染毒PC12细胞模型,实验设对照组、Rot染毒组、HN预处理Rot染毒组、单独HN处理组。采用ELISA检测Rot染毒细胞内外HN的含量,CCK-8法... 详细信息

目的探讨humanin(HN)对鱼藤酮(rotenone,Rot)诱导的多巴胺神经元毒性损伤的保护作用和机制。方法构建Rot染毒PC12细胞模型,实验设对照组、Rot染毒组、HN预处理Rot染毒组、单独HN处理组。采用ELISA检测Rot染毒细胞内外HN的含量,CCK-8法检测细胞活性,ATP检测试剂盒检测细胞内ATP含量,DCFH-DA探针检测细胞内ROS水平,Western blot分别检测线粒体自噬调控蛋白Pink1、Parkin、p-Parkin、p62、LC3,线粒体生物发生调控蛋白PGC1α和分裂/融合调控蛋白OPA1、MFN2、DRP1、p-DRP1以及抗氧化应激调控蛋白Keap1、Nrf2的表达。采用HBAD-mcherry-EGFP-LC3腺病毒转染细胞观察自噬体和自噬溶酶体的数量。结果Rot染毒组PC12细胞内HN浓度显著高于对照组(P<0.05);与对照组比较,Rot染毒组PC12细胞活性下降,ATP含量下降,ROS的生成增加,Rot染毒后PC12细胞内Pink1、p-Parkin表达升高,LC3Ⅱ/LC3Ⅰ比值升高,p62表达下降,细胞线粒体生物发生蛋白PGC1α和线粒体融合蛋白MFN2、OPA1表达下降,而线粒体分裂蛋白p-DRP1表达升高,抗氧化应激蛋白Keap1和Nrf2表达下降(P均<0.05);与对照组比较,Rot染毒组PC12细胞中自噬体和自噬溶酶体数量增多(P<0.05),而20μmol/L HN预处理可以改善Rot染毒引起的上述变化(P<0.05)。结论HN通过抑制线粒体自噬和线粒体分裂、促进线粒体生物发生和融合以及抗氧化应激,改善Rot诱导的多巴胺神经元毒性损伤。

关键词： humanin 鱼藤酮多巴胺神经元线粒体

humanin抑制NR1亚基表达和NR2B亚基磷酸化的神经保护作用

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吉林大学学报（医学版） 2012年第5期38卷 907-911,I0001页

作者：翁启芳龙儒桃许闽广王丹妹张策海南医学院生理学教研室海南海口571199 海南医学院病理生理学教研室海南海口571199 海南医学院机能学实验室海南海口571199 山西医科大学生理学系山西太原030001

目的:探讨humanin(HN)通过抑制N-甲基-D-天门冬氨酸(NMDA)受体NR1亚基的表达和NR2B亚基的磷酸化在兴奋性神经毒中发挥的保护作用,并阐明其可能的作用机制。方法:利用原代培养的Wistar大鼠皮层神经元建立NMDA诱导的兴奋性神经毒模型,将... 详细信息

目的:探讨humanin(HN)通过抑制N-甲基-D-天门冬氨酸(NMDA)受体NR1亚基的表达和NR2B亚基的磷酸化在兴奋性神经毒中发挥的保护作用,并阐明其可能的作用机制。方法:利用原代培养的Wistar大鼠皮层神经元建立NMDA诱导的兴奋性神经毒模型,将神经元分为对照组、NMDA组、NMDA+MK-801(MK-801)组和NMDA+HN(HN)组。流式细胞术荧光定量检测各组神经元膜NMDA受体NR1亚基蛋白的表达,Western blotting法检测各组神经元膜NMDA受体NR2B亚基Tyr1472位点的磷酸化水平。结果:倒置相差显微镜观察,NMDA组中的神经元胞体肿胀,个别细胞变成圆形,胞体周围光晕模糊,神经元突起大部分消失,表现出明显的神经毒性作用。流式细胞术免疫荧光定量检测,与对照组比较,NMDA组NR1亚基蛋白的平均荧光强度值明显增加(P<0.05);与NMDA组比较,MK-801组和HN组的NR1亚基蛋白的平均荧光强度值明显降低(P<0.05)。Western blotting法检测,各组神经元的NR2B亚基总蛋白的表达水平无改变;与对照组比较,NMDA组NR2B亚基蛋白Tyr1472位点的磷酸化水平明显升高(P<0.05);与NMDA组比较,MK-801组和HN组均能降低NR2B亚基蛋白Tyr1472位点的磷酸化水平(P<0.05)。结论:NMDA受体NR1亚基蛋白表达水平的增加和NR2亚基磷酸化可能参与NMDA诱导的兴奋性神经毒作用;HN可能通过抑制NR1亚基的表达和NR2B亚基的磷酸化而发挥对神经元的保护作用。

关键词： humanin N-甲基-D-天门冬氨酸受体 NR1亚基 NR2B亚基兴奋性神经毒

humanin拮抗AD相关毒性作用的研究进展

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生理科学进展 2006年第4期37卷 302-306页

作者：崔爱玲赵丽李灵敏乔健天张策山西医科大学生理学教研室太原030001

阿尔采末病(A lzheimer's d isease,AD)严重威胁着老年人的健康与生存质量,由于其发病原因复杂、机制不明,目前尚缺乏有效的防治措施。humanin是近年来发现的能特异性抑制AD相关毒性的分泌性短肽,通过自身二聚化在细胞外发挥神经保护作... 详细信息

阿尔采末病(A lzheimer's d isease,AD)严重威胁着老年人的健康与生存质量,由于其发病原因复杂、机制不明,目前尚缺乏有效的防治措施。humanin是近年来发现的能特异性抑制AD相关毒性的分泌性短肽,通过自身二聚化在细胞外发挥神经保护作用。humanin通过直接或间接作用抑制β-淀粉样蛋白(Aβ),以及家族性AD(FAD)基因如早老基因突变诱发的神经毒,而对AD不相关的毒性作用如凋亡诱导剂etoposide及Fas诱导的细胞死亡却不表现拮抗作用。因此,humanin可通过特异性拮抗AD相关的神经毒而发挥重要的神经保护作用。

关键词： humanin 神经保护阿尔采末病 β-淀粉样蛋白神经毒

Science Letters:Construction of a eukaryotic expression plasmid of humanin

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2005年第1期6卷 11-13页

作者：罗本燕陈祥明唐敏陈峰陈智 Department of Neurology First Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhou310003China Department of Anesthesiology Second Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhou310009China Institute of Infectios Diseases.First Affiliated Hospital School of MedicineZhejiang UniversityHangzhou310001.China

Objective:To construct a eukaryotic expression plasmid pcDNA3.1(-)-***:The recombinant plasmidpGEMEX-1-humanin was digested with restriction endonucleases BamH Ⅰ and Hind Ⅲ and the humanin gene fragments,about100 bp length,were *** the humanin gene fragments were inserted into eukaryotic expression vector pcDNA3.1(-)andthe recombinant plasmids pcDNA3.1(-)-humanin were identified by ***:Recombinant plasmid DNA success-fully produced a band which had the same size as that of the thimauin positive *** sequence of recombinant plasmidsaccorded with the Humnain gene ***:A eukaryotic expression plasmid of humanin was successfully con-structed.

关键词： humanin Alzheimer's disease Eukaryotic expression

humanin在代谢性疾病作用中的研究进展

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中国病理生理杂志 2024年第9期40卷 1736-1743页

作者：姜枫姚婷婷衣雪洁高海宁沈阳体育学院辽宁沈阳110002

发病率逐年增高的代谢性疾病对人们的生命安全造成极大威胁,寻找治疗代谢性疾病的有效靶点成为了亟待解决的问题。humanin(HN)是一种由线粒体DNA转录翻译的具有24个氨基酸的线性多肽,过去的研究表明它具有神经细胞保护作用。近年来的研... 详细信息

发病率逐年增高的代谢性疾病对人们的生命安全造成极大威胁,寻找治疗代谢性疾病的有效靶点成为了亟待解决的问题。humanin(HN)是一种由线粒体DNA转录翻译的具有24个氨基酸的线性多肽,过去的研究表明它具有神经细胞保护作用。近年来的研究发现HN与机体的糖脂代谢调节密切相关,并且在动物实验中使用HN或HN类似物可以有效治疗多种代谢性疾病。因此,本文回顾了HN的基础生物学功能与信号传导机制,并系统全面地总结了HN在2型糖尿病、非酒精性脂肪性肝病、动脉粥样硬化和多囊卵巢综合征中的作用机制与治疗效果,旨在探讨HN作为代谢性疾病防治靶点的潜力。

关键词： humanin 代谢性疾病 2型糖尿病非酒精性脂肪性肝病动脉粥样硬化多囊卵巢综合征

humanin通过内源性途径抑制Aβ_(31-35)诱导的神经元凋亡(英文)

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生理学报 2010年第2期62卷 93-100页

作者：李灵敏张宇乔建天张策山西医科大学病理学教研室太原030001 山西医科大学生理学教研室太原030001

为了探讨humanin(HN)对Aβ31-35诱导的培养皮层神经元凋亡的影响,本研究采用不同浓度(5、10、20μmol/L)的HN预孵育体外培养的皮层神经元不同时间(0、8、16h),加入Aβ31-35(25μmol/L)24h后,应用电子显微镜观察神经元的凋亡情况;流式细... 详细信息

为了探讨humanin(HN)对Aβ31-35诱导的培养皮层神经元凋亡的影响,本研究采用不同浓度(5、10、20μmol/L)的HN预孵育体外培养的皮层神经元不同时间(0、8、16h),加入Aβ31-35(25μmol/L)24h后,应用电子显微镜观察神经元的凋亡情况;流式细胞术、TUNEL法检测神经元的凋亡率;酶标仪检测caspase活性;Westernblot检测Bax蛋白的表达。结果显示:HN(20μmol/L)预孵育16h明显抑制了Aβ31-35诱导的神经元凋亡;HN降低了Aβ31-35诱导的caspase-3、9活性的升高;HN抑制了Aβ31-35诱导的Bax从胞浆到线粒体的转位。以上结果提示,HN通过阻断内源性凋亡途径抑制Aβ31-35诱导的神经元凋亡。

关键词： Aβ31-35 humanin 凋亡神经保护内源性途径