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bnip3 acts as transcriptional repressor of death receptor-5 expression and prevents TRAIL-induced cell death in gliomas

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CELL DEATH & DISEASE 2013年第4期4卷 e587-e587页

作者： Burton, T. R. Henson, E. S. Azad, M. B. Brown, M. Eisenstat, D. D. Gibson, S. B. Univ Manitoba Dept Biochem Winnipeg MB R3E 0V9 Canada Univ Manitoba Dept Med Genet Winnipeg MB R3E 0V9 Canada Univ Manitoba Manitoba Inst Cell Biol Winnipeg MB R3E 0V9 Canada Univ Manitoba Dept Pediat Winnipeg MB R3E 0V9 Canada Univ Manitoba Dept Child Hlth Winnipeg MB R3E 0V9 Canada Univ Manitoba Dept Human Anat Winnipeg MB R3E 0V9 Canada Univ Manitoba Dept Cell Sci Winnipeg MB R3E 0V9 Canada

Glioblastoma multiforme (GBM) is the most common and malignant brain tumor, and current treatment modalities such as surgical resection, adjuvant radiotherapy and temozolomide (TMZ) chemotherapy are ineffective. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a novel cancer therapeutic agent for GBM because of its capability of inducing apoptosis in glioma cells. Unfortunately, the majority of glioma cells are resistant to TRAIL-induced apoptosis. The Bcl-2 nineteen kilodalton interacting protein (bnip3) is a pro-cell death BH3-only member of the Bcl-2 family that is one of the highest expressed genes in hypoxic regions of GBM tumors. We previously found that bnip3 is localized to the nucleus in GBM tumors and suppresses cell death in glioma cells. Herein, we have discovered when bnip3 nuclear expression is knockdown in glioma cell lines and in normal mouse astrocytes, TRAIL and its death receptor, death receptor-5 (DR5) expression is increased. In addition, when nuclear bnip3 expression is increased, the amount of TRAIL-induced apoptosis is reduced. Using a streptavidin pull-down assay, we found that bnip3 binds to the DR5 promoter and nuclear bnip3 binds to the DR5 promoter. Furthermore, nuclear bnip3 expression in GBM tumors correlates with decreased DR5 expression. Taken together, we have discovered a novel transcriptional repression function for bnip3 conferring a TRAIL resistance in glioma cells. Cell Death and Disease (2013) 4, e587;doi:10.1038/cddis.2013.100;published online 11 April 2013

关键词： bnip3 TRAIL gliomas DR5 apoptosis

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bnip3 subfamily BH3-only proteins: mitochondrial stress sensors in normal and pathological functions

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ONCOGENE 2008年第12-2-2008期27卷 S114-S127页

作者： Chinnadurai, G. Vijayalingam, S. Gibson, S. B. St Louis Univ Sch Med Inst Mol Virol Doisy Res CtrMed Ctr St Louis MO 63104 USA Univ Manitoba Manitoba Inst Cell Biol Winnipeg MB Canada

The bnip3 subfamily of BH3-only proteins consists of bnip3 and bnip3-like (bnip3L) proteins. These proteins form stable homodimerization complexes that localize to the outer membrane of the mitochondria after cellular stress. This promotes either apoptotic or non-apoptotic cell death such as autophagic cell death. Although the mammalian cells contain both members of this subfamily, the genome of Caenorhabditis elegans codes for a single bnip3 ortholog, cebnip3, which shares homology in the transmembrane (TM) domain and in a conserved region close to the BH3 domain of mammalian bnip3 protein. The cell death activities of bnip3 and bnip3L are determined by either the BH3 domain or the C-terminal TM domain. The TM domain of bnip3 is unique, as it is capable of autonomous stable dimerization and contributes to mitochondrial localization of bnip3. In knockout mouse models, bnip3L was shown to be essential for normal erythrocyte differentiation and hematopoietic homeostasis, whereas bnip3 plays a role in cellular responses to ischemia/reperfusion injury in the heart. Both bnip3 and bnip3L play a role in cellular responses to stress. Under hypoxia, both bnip3 and bnip3L expression levels are elevated and contribute to hypoxia-induced cell death. In addition, these proteins play critical roles in disease states. In heart disease, both bnip3 and bnip3L play a critical role in cardiomyocyte cell death following ischemic and non-ischemic injuries. In cancer, expression of bnip3 and bnip3L is downregulated by promoter hypermethylation or by homozygous deletion of the gene locus in certain cancers, whereas their expression was increased in other cancers. In addition, bnip3 expression has been correlated with poor prognosis in some cancers. The results reviewed here suggest that bnip3 and bnip3L may be novel therapeutic targets for intervention because of their pathological roles in regulating cell death in disease states. Oncogene (2009) 27, S114-S127;doi: 10.1038/onc.2009.49

关键词： bnip3 bnip3L apoptosis autophagy cancer cardiomyopathies

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bnip3: a new cell death pathway regulating necrosis?

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Arthritis Research & Therapy 2000年第1期3卷 1-3页

作者： Corinne Guingamp Center of Experimental Rheumatology Zurich Switzerland

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bnip3-AIF pathway is involved in hippocampal neuronal death induced by oxygen-glucose deprivation

BNIP3-AIF pathway is involved in hippocampal neuronal death ...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Shen-Ting ZHAO~1,Ming CHEN~1,Shu-Ji LI~1,Ming-Hai ZHANG~1,Bo-Xing LI~1,Xin-Hong ZHU~1,Ji-Ming KONG~(1,2),Tian-Ming GAO~(1,*) 1 Department of Neurobiology,Southern Medical University,Guangzhou 510515,China 2 Department of Human Anatomy and Cell Science,University of Manitoba Faculty of Medicine,Winnipeg,Man., Canada

Objective Evidences have shown that mitochondrial protein apoptosis-inducing factor(AIF) is involved in caspase-independent neuronal apoptosis induced by ***,its upstream signaling mechanism remains *** we test the hypothesis that bnip3 may be an upstream signal of AIF that mediates ischemic neuronal death. Methods We performed immunocytochemistry,Western blotting,cell transfection,subcellular fractionation,and RNA interfering to analyze the expression and localization of BNTP3 and AIF in primary cultured hippocampal neurons subjected to oxygen-glucose deprivation(OGD).Results After OGD,both bnip3 and AIF are *** translocates from mitochondria to nucleus in a time-dependent manner which follows the mitochondrial bnip3 ***,the translocation of AIF occurs hours before the observable nuclear *** of bnip3 induces nuclear translocation of AIF and the neuronal death whereas inhibition of bnip3 decreases OGD-induced AIF translocation and neuronal ***3-induced neuronal death is also blocked by reducing AIF *** bnip3-AIF pathway is involved in OGD-induced hippocampal neuronal death.

关键词： oxygen-glucose deprivation hippocampal neuron apoptosis bnip3 AIF

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miR-31-5p对牙髓干细胞HIF-1α/bnip3信号通路及成骨相关因子表达的影响

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上海口腔医学 2022年第3期31卷 237-242页

作者：付洪海孙乐刚丁昌成马向瑞黄玉梅滨州医学院附属医院口腔颌面外科山东滨州256603 滨州医学院附属医院药学部山东滨州256603 滨州医学院附属医院口腔修复科山东滨州256603

目的 :探讨微小RNA-31-5p(miR-31-5p)对牙髓干细胞(DPSCs)低氧诱导因子1α(HIF-1α)/Bcl-2/腺病毒E1B 19-kDa相互作用蛋白3(bnip3)信号通路及成骨相关因子表达的影响。方法 :体外培养人DPSCs,分为对照组(不转染)、mimic NC组(转染negati... 详细信息

目的 :探讨微小RNA-31-5p(miR-31-5p)对牙髓干细胞(DPSCs)低氧诱导因子1α(HIF-1α)/Bcl-2/腺病毒E1B 19-kDa相互作用蛋白3(bnip3)信号通路及成骨相关因子表达的影响。方法 :体外培养人DPSCs,分为对照组(不转染)、mimic NC组(转染negative control-miR-31-5p)、miR-31-5p mimic组(转染hsa-miR-31-5p mimic)、si RNA NC组(转染nonsense siRNA)和miR-31-5p siRNA组(转染miR-31-5p siRNA)。实时荧光定量PCR(qRT-PCR)检测各组DPSCs细胞中miR-31-5p、HIF-1α、bnip3、碱性磷酸酶(ALP)、Runt相关转录子2(Runx2)mRNA的表达情况,MTT法检测各组DPSCs细胞增殖情况,ALP活性测定试剂盒检测各组DPSCs细胞ALP活性,蛋白印迹(WB)法检测各组DPSCs细胞中HIF-1α、bnip3、Runx2蛋白的表达情况。采用SPSS 24.0软件包对数据进行统计学分析。结果:与对照组、mimic NC组相比,miR-31-5p mimic组DPSCs细胞A值、ALP mRNA表达水平及活性、Runx2 mRNA及蛋白表达水平显著降低(P<0.05),ALP染色明显减弱,miR-31-5p mRNA、HIF-1α、bnip3 mRNA及HIF-1α、bnip3、Beclin1蛋白表达水平显著升高(P<0.05)。与对照组、siRNA NC组相比,miR-31-5p siRNA组DPSCs细胞A值、ALP mRNA表达水平及活性、Runx2 mRNA及蛋白水平显著升高(P<0.05),ALP染色明显增强,miR-31-5p mRNA、HIF-1α、bnip3 mRNA及HIF-1α、bnip3、Beclin1蛋白表达水平显著降低(P<0.05)。结论 :miR-31-5p可以激活HIF-1α/bnip3信号通路,抑制DPSCs细胞的成骨相关因子表达。

关键词：微小RNA-31-5p 牙髓干细胞 HIF-1α bnip3 成骨相关因子表达

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兔退变椎间盘中髓核细胞凋亡与bnip3基因表达的意义

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中国修复重建外科杂志 2010年第11期24卷 1367-1371页

作者：曾顺福刘杰王建第三军医大学新桥医院骨科重庆400037

目的髓核细胞凋亡可能与髓核组织代谢障碍产生缺氧,导致bnip3基因表达有关。通过观察兔退变椎间盘中髓核组织的细胞密度、细胞凋亡率及bnip3的表达,为进一步了解髓核细胞凋亡机制提供实验依据。方法健康3月龄雄性新西兰大白兔30只,体重(... 详细信息

目的髓核细胞凋亡可能与髓核组织代谢障碍产生缺氧,导致bnip3基因表达有关。通过观察兔退变椎间盘中髓核组织的细胞密度、细胞凋亡率及bnip3的表达,为进一步了解髓核细胞凋亡机制提供实验依据。方法健康3月龄雄性新西兰大白兔30只,体重(2.3±0.2)kg,随机分为实验组(n=20)及对照组(n=10)。实验组大白兔采用针刺L3、4、L4、5及L5、6椎间盘制备椎间盘退变模型;对照组仅暴露椎间盘后缝合。术后4、8周通过MRI检查评价椎间盘退变情况,采用组织学观察和TUNEL法检查椎间盘髓核组织中凋亡细胞,用免疫组织化学染色法检测兔椎间盘髓核细胞bnip3的表达。结果 MRI检查示实验组术后4、8周椎间盘髓核信号强度呈逐渐降低趋势。根据Pfirrmann分级标准,实验组术后4、8周椎间盘退变分级比较,差异均有统计学意义(P<0.05)。组织学观察及TUNEL检查示:对照组椎间盘髓核中细胞密度高,可见少量散在的凋亡细胞;实验组术后4、8周时椎间盘髓核组织内细胞密度逐渐降低,可见较多凋亡细胞。各时间点实验组细胞密度、TUNEL染色阳性细胞率与对照组比较,以及实验组各指标两时间点间比较,差异均有统计学意义(P<0.05)。对照组椎间盘髓核组织细胞中无bnip3表达;实验组术后4、8周椎间盘髓核组织细胞中bnip3表达逐渐增多,bnip3染色阳性细胞率分别为13.45%±1.16%、32.00%±1.82%,bnip3灰度值分别为194.32±4.65、117.54±2.11,各时间点间比较差异均有统计学意义(P<0.05)。结论椎间盘退变与髓核组织中细胞密度下降有关,细胞凋亡是椎间盘髓核细胞减少的原因之一,bnip3参与了椎间盘髓核细胞凋亡。

关键词：椎间盘退变髓核组织细胞凋亡 bnip3 MRI 兔

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肾透明细胞癌组织中bnip3的表达及意义

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四川大学学报（医学版） 2014年第3期45卷 396-399页

作者：黄龙赵涛田义阳王海舟陈雪芹徐苗李响四川大学华西医院泌尿外科成都610041 四川大学华西医院病理科成都610041

目的研究肾透明细胞癌中bnip3表达及意义。方法收集肾癌手术切除的肾癌组织和对应癌旁正常肾组织新鲜标本,共30例。运用实时荧光定量PCR、蛋白质印迹法(Western blot)检测各组bnip3、von Hippel-Lindan(VHL)、缺氧诱导因子-1α(HIF-1α... 详细信息

目的研究肾透明细胞癌中bnip3表达及意义。方法收集肾癌手术切除的肾癌组织和对应癌旁正常肾组织新鲜标本,共30例。运用实时荧光定量PCR、蛋白质印迹法(Western blot)检测各组bnip3、von Hippel-Lindan(VHL)、缺氧诱导因子-1α(HIF-1α)、血管内皮生长因子(VEGF)的表达情况。并分析bnip3与VHL、HIF-1α、VEGF表达相关性,及各个基因表达与临床病理参数间关系。结果实时荧光定量PCR检测结果示:在RNA水平,bnip3、VHL在肾癌组织中表达水平低于癌旁正常肾组织(P<0.05),HIF-1α和VEGF在肾癌组织中表达水平高于癌旁正常肾组织(P<0.05),bnip3表达与VHL、HIF-1α、VEGF无相关性,肾癌组织中bnip3低表达与各个临床病理学特征无相关性。Western blot检测结果示:在蛋白水平,bnip3、VHL在肾癌组织中表达水平低于癌旁正常肾组织(P<0.05),HIF-1α和VEGF在肾癌组织中表达水平高于癌旁正常肾组织(P<0.05)。bnip3蛋白表达与VHL、HIF-1α、VEGF蛋白亦无相关性(P>0.05)。结论可能存在某种调控机制使bnip3在肾透明细胞癌表达下调,且bnip3低表达与VHL、HIF-1α、VEGF表达无相关性。

关键词：肾透明细胞癌 bnip3 缺氧诱导因子-1α 血管内皮生长因子实时荧光定量PCR 蛋白质印迹法

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bnip3 mediates doxorubicin-induced cardiomyocyte pyroptosis via caspase-3/GSDME

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LIFE SCIENCES 2020年第0期242卷 117186-000页

作者： Zheng, Xinbin Zhong, Ting Ma, Yeshuo Wan, Xiaoya Qin, Anna Yao, Bifeng Zou, Huajiao Song, Yan Yin, Deling Cent S Univ Xiangya Sch Pharmaceut Sci Changsha 41008 Hunan Peoples R China East Tennessee State Univ Dept Internal Med Coll Med Johnson City TN 37614 USA Zhengzhou Univ Affiliated Hosp 1 Dept Vasc Surg Zhengzhou 450052 Henan Peoples R China

Aims: This study was aimed to investigate the role of GSDME-mediated pyroptosis in cardiac injury induced by Doxorubicin (DOX), and to evaluate the role of BH3-only protein Bcl-2/adenovirus E1B 19-kDa-interacting protein 3 (bnip3) in regulation of DOX-induced pyroptosis. Main methods: HL-1 cardiomyocytes and C57BL/6J mice were treated by DOX to establish DOX-induced cardiotoxicity in vitro and in vivo models, respectively. Cell transfection was applied to regulate the expression of caspase-3, GSDME and bnip3. Western blot was used for measuring expression of protein level. LDH-cytotoxicity assay was used to detect the LDH release. The Flow cytometry analysis was used to detect the cell death. Echocardiography was used to determine the cardiac function. HE staining was used for observing pathological feature of heart tissues. Key findings: Our results showed that GSDME-mediated pyroptosis was involved in DOX-induced cardiotoxicity in vivo. We showed that HL-1 cardiomyocytes exposed to DOX exhibited morphological features of pyroptosis in vitro. We also showed that DOX induced activation of caspase-3 and eventually triggered GSDME-dependent pyroptosis, which was reduced by the silence or inhibitor of caspase-3. We further showed that knockdown of GSDME inhibited DOX-induced cardiomyocyte pyroptosis in vitro. Finally, DOX increased the expression of bnip3, whereas silencing of bnip3 blunted cardiomyocyte pyroptosis induced by DOX, which was regulated through caspase-3 activation and GSDME cleavage. Significance: Our findings revealed a novel pathway that cardiomyocyte pyroptosis is regulated through bnip3-caspase-3-GSDME pathway following DOX treatment, suggesting that bnip3-dependent pyroptosis may offer a novel therapeutic strategy to reduce cardiotoxicity induced by DOX.

关键词： Pyroptosis bnip3 GSDME Caspase-3 Doxorubicin

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bnip3介导退变性髓核细胞死亡信号转导的研究

BNIP3介导退变性髓核细胞死亡信号转导的研究

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作者：刘杰第三军医大学

学位级别：博士

研究背景椎间盘退变性疾病是骨科最常见病种之一，不仅为患者及家庭带来了痛苦，也给社会造成了极大的经济负担。椎间盘退变过程中，椎间盘组织显示出明显的组织结构学改变，比如髓核组织脱水、细胞死亡、纤维环断裂及终板软骨钙化变薄... 详细信息

研究背景椎间盘退变性疾病是骨科最常见病种之一，不仅为患者及家庭带来了痛苦，也给社会造成了极大的经济负担。椎间盘退变过程中，椎间盘组织显示出明显的组织结构学改变，比如髓核组织脱水、细胞死亡、纤维环断裂及终板软骨钙化变薄等。与此同时，椎间盘内的营养代谢也发生了显著改变，目前研究证实，在椎间盘退变过程中，髓核细胞的死亡与营养代谢有着密切关系。 bnip3蛋白是目前已知的与营养代谢有关的促细胞死亡蛋白之一，通常情况下在细胞内不表达或低表达，当细胞应激时，bnip3蛋白表达上调，并与线粒体外膜相结合，导致线粒体膜电位丧失、通透性增加、线粒体内促死亡蛋白释放，最终诱导细胞死亡。凋亡诱导因子（AIF）是目前已知的诱导非经典性细胞死亡的蛋白之一，正常情况下存在于线粒体基质内，当线粒体外膜通透性增加，AIF从线粒体内释放并转位细胞核，导致细胞核发生大片段DNA断裂。因此，我们假设当椎间盘发生退变时，局部髓核组织内营养代谢发生显著改变，bnip3蛋白表达异常增加，最终通过经典的和/或非经典的细胞死亡通路导致髓核细胞死亡。目的证实bnip3蛋白参与了退变性椎间盘髓核细胞死亡，通过抑制bnip3蛋白表达可以延缓甚至中断椎间盘髓核细胞死亡，由此阻止椎间盘退变的进一步发展，为退变性椎间盘疾病的生物治疗提供新的理论依据。方法 1．大鼠尾椎间盘髓核细胞的体外分离培养及鉴定取健康SD大鼠尾椎间盘髓核细胞，在含有10%灭活FBS的DMEM/F12培养液中培养，倒置相差显微镜下观察原代细胞形态，爬片培养后进行甲苯胺蓝、HE、聚集蛋白聚糖和II型胶原免疫组织化学染色，透射电镜观察，对髓核细胞体外的生物学特性进行研究。 ***3在退变性髓核细胞中表达的实验研究体外通过营养剥夺（无糖、无血清、低氧）模拟体内椎间盘退变微环境，测定在正常培养环境及营养剥夺培养环境下，髓核细胞死亡率、线粒体膜电位、Caspase酶活性变化以及bnip3、AIF表达量改变及其细胞内定位。 3．髓核细胞bnip3过表达及抑制实验通过构建慢病毒载体，在髓核细胞内分别过表达及抑制bnip3蛋白，通过免疫细胞化学及细胞器蛋白定量技术，分析bnip3蛋白与髓核细胞死亡之间的联系及其机制。 4．动物模型实验构建椎间盘退变动物模型，建模后即刻、2周、4周及8周，通过MRI及椎间盘组织学染色评估椎间盘退变效果，利用免疫组织化学及PCR技术，分析bnip3蛋白表达与椎间盘退变之间的关系。结果 1．大鼠尾椎间盘髓核细胞生物学特性 1.1大鼠尾椎间盘髓核细胞：1、倒置显微镜下观察，原代大鼠尾椎间盘髓核细胞呈类圆形，体积较大，折光强，5d始有细胞贴壁，细胞呈多角形或短梭形，12d14d细胞生长进入指数期，约21d时，细胞长满瓶壁，可进行传代；2、大鼠尾椎间盘髓核细胞活力测定，初次分离时细胞活力约95%～97%，原代培养期间，细胞活力维持在98%～100%，第一次传代后，细胞活力仍保持98%100%；3、大鼠尾椎间盘髓核细胞行甲苯胺蓝染色显示强阳性，HE组织学染色显示细胞核、细胞质着色明显，界限清晰，II型胶原蛋白、聚集蛋白聚糖免疫细胞化学染色呈阳性；4、细胞透射电镜显示原代大鼠尾椎间盘髓核细胞内线粒体少，细胞质内有大量糖原颗粒。 1.2通过对大鼠尾椎间盘髓核细胞的培养及观察，原代细胞取材容易，但分离出的细胞较少，生长缓慢，而传代后髓核细胞生长速度加快，数量多，适合进一步实验需要，因此后续实验均采用第一代的髓核细胞进行。 2．营养剥夺诱导髓核细胞bnip3表达及AIF细胞核转位 real-time PCR、细胞免疫荧光染色及Western Blot显示对照组细胞低表达bnip3，蛋白主要位于胞浆，实验组显示随营养剥夺时间延长，bnip3表达呈上升趋势，在48h明显增加，且bnip3与线粒体相结合；流式细胞仪检测发现细胞死亡及线粒体膜电位在正常对照组无明显变化，而在实验组随培养时间延长细胞死亡增加、膜电位降低。与此同时，实验组组研究发现，线粒体基质内的AIF蛋白表达虽然未发生明显改变，但AIF逐渐从线粒体基质中释放出来并转移至细胞核内。 3．过表达及抑制bnip3蛋白对髓核细胞的影响 3.1通过体外构建慢病毒及RNA干扰技术，实现细胞内bnip3蛋白过表达及表达抑制，发现：1、bnip3过表达可急剧降低细胞在退变环境中的生存率，而细胞死亡显著增加；2、通过RNAi抑制bnip3蛋白表达后，可增强细胞在退变环境下的耐受性，增加细胞活性。 3.2bnip3过表达及抑制实验时，通过细胞器AIF蛋白定量检测发现：1、BNI

关键词：髓核细胞细胞死亡信号转导椎间盘退变 bnip3 AIF 线粒体

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Antigen processing and presentation-related signature-derived bnip3 is a novel oncogene and immunotherapy determinant in osteosarcoma based on machine learning and in vitro validation

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JOURNAL OF GENE MEDICINE 2024年第1期26卷 e3586-e3586页

作者： Chen, Yang Cao, Yajie Wu, Song Cao, Xu Cai, Ting Hu, Hai Cent South Univ Xiangya Hosp 3 Dept Orthoped Changsha Peoples R China Cent South Univ Xiangya Hosp 3 Ctr Clin Pharmacol Changsha Peoples R China Cent South Univ Xiangya Hosp 3 Dept Gastroenterol Changsha Peoples R China

Background: In recent decades, osteosarcoma has remained the most prevalent kind of malignant tumor. An important and crucial factor in immunotherapy is antigen processing and presentation (APP). The specific functions and pathogenic processes of APP in osteosarcoma have not, however, been ***: Patients with osteosarcoma were divided into groups using APP-related genes. Machine learning was used to further build the APP-related score. Investigated in-depth were the prognostic relevance of the score, mutation features, immunological aspects, and pharmacological prediction performance. Investigations of the prognostic utility, immunological traits, drug prediction effectiveness and immunotherapy prediction of bnip3 were performed ***: Investigations by cell counting kit-8, Transwell and 5-ethynyl-2-deoxyuridine (EdU) demonstrated that bnip3 is an osteosarcoma tumor accelerator. The osteosarcoma gene bnip3 may promote macrophage migration. The APP-related score shows potential for clinical ***: It was anticipated that more in vitro and in vivo studies would confirm bnip3's tumorigenic and immunogenic processes in osteosarcoma.

关键词： bnip3 immunotherapy machine learning osteosarcoma tumor microenvironment

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