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Arsenic trioxide induces autophagic cell death in malignant glioma cells by upregulation of mitochondrial cell death protein bnip3

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ONCOGENE 2005年第6期24卷 980-991页

作者： Kanzawa, T Zhang, L Xiao, LC Germano, IM Kondo, Y Kondo, S Univ Texas MD Anderson Canc Ctr Dept Neurosurg Unit 64 Houston TX 77030 USA Univ Texas MD Anderson Canc Ctr Dept Biostat Houston TX 77030 USA Mt Sinai Sch Med Dept Neurosurg New York NY 10510 USA

Arsenic trioxide (As2O3) has shown considerable efficacy in treating hematological malignancies with induction of programmed cell death (PCD) type I, apoptosis. However, the mechanisms underlying the antitumor effect of As2O3 on solid tumors are poorly defined. Previously, we reported that As2O3 induced autophagic cell death (PCD type II) but not apoptosis in human malignant glioma cell lines. The purpose of this study was to elucidate the molecular pathway leading to autophagic cell death. In this study, we demonstrated that the cell death was accompanied by involvement of autophagy-specific marker, microtubule-associated protein light chain 3 (LC3), and damage of mitochondrial membrane integrity, but not by caspase activation. Analysis by cDNA microarray, RT-PCR, and Western blot showed that cell death members of Bcl-2 family, Bcl-2/adenovirus E1B 19-kDa- interacting protein 3 (bnip3) and its homologue bnip3-like (bnip3L), were upregulated in As2O3-induced autophagic cell death. Exogenous expression of bnip3, but not bnip3L, induced autophagic cell death in malignant glioma cells without As2O3 treatment. When upregulation of bnip3 induced by As2O3 was suppressed by a dominant-negative effect of the transmembrane-deleted bnip3 (bnip3DTM), autophagic cell death was inhibited. In contrast, bnip3 transfection augmented As2O3-induced autophagic cell death. These results suggest that bnip3 plays a central role in As2O3-induced autophagic cell death in malignant glioma cells. This study adds a new concept to characterize the pathways by which As2O3 acts to induce autophagic cell death in malignant glioma cells.

关键词： arsenic trioxide autophagy bnip3 glioma LC3

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Membrane translocation and oligomerization of hBok are triggered in response to apoptotic stimuli and bnip3

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CELLULAR AND MOLECULAR LIFE SCIENCES 2005年第9期62卷 1015-1024页

作者： Gao, S Fu, W Dürrenberger, M De Geyter, C Zhang, H Univ Basel Dept Res CH-4031 Basel Switzerland Univ Basel Univ Womens Hosp CH-4031 Basel Switzerland Univ Zurich Hosp Med Res Ctr CH-8091 Zurich Switzerland Univ Basel Bioctr CH-4031 Basel Switzerland

hBok is a human pro-apoptotic member of the Bcl-2 family. By fluorescence in situ hybridization and in silico analysis, hBok was found to be located on chromosome 2q37.3. Its expression was detected in various organs and several hormonally regulated cancer cells. Expression of hBok was shown to be upregulated in estrogen-dependent breast cancer by estrogen deprivation and in myocardial cells during hypoxia. Confocal laser scanning microscopy examinations and subcellular fractionation studies showed that hBok was distributed in both the cytosol and intracellular membranes of healthy cells. Upon overexpression of hBok or stimulation of apoptosis, hBok became integrated into the membrane. Furthermore, apoptosis and oligomerization were promoted by BH3-only proteins, such as Bid, bnip3 and p53, but prevented by BFL-1. hBok was found to interact with bnip3. Our findings suggest that functional BH3-only proteins facilite the oligomerization and insertion of hBok into the membrane to activate it.

关键词： hBok apoptosis bnip3 subcellular localization oligomerization

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Placental localization and expression of the cell death factors bnip3 and Nix in preeclampsia, intrauterine growth retardation and HELLP syndrome

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EUROPEAN JOURNAL OF OBSTETRICS & GYNECOLOGY AND REPRODUCTIVE BIOLOGY 2005年第2期122卷 172-176页

作者： Stepan, H Leo, C Purz, S Höckel, M Horn, LC Univ Leipzig Dept Obstet & Gynecol D-04103 Leipzig Germany Univ Leipzig Inst Pathol Div Gynecol & Perinatal Pathol D-04103 Leipzig Germany

Objective: bnip3 and its homologue Nix are pro-apoptotic factors of the Bcl-2-family and are expressed in malignant tumors. In vitro, this expression was shown to be mediated by hypoxia. Recently, it has been shown that placental hypoxia as well as apoptosis are pathogenetic factors for pregnancy-induced hypertensive diseases and intrauterine growth retardation (IUGR). The aim of the study was to analyze placental expression of bnip3 and Nix in pregnancies complicated by preeclampsia, hemolysis, elevated liver enzymes and low platelets (HELLP) syndrome and IUGR. Material and methods: Placental tissue was sampled from 10 pregnancies each with preeclampsia, HELLP syndrome, IUGR and gestational age-matched controls. The placental expression of bnip3/Nix has been investigated with immunohistochemistry by the use of specific human bnip3/Nix antibodies. Results: In cytotrophoblastic cells, the bnip3 expression was strong in the control placentas, but only mediate in the placentas from pregnancies with preeclampsia, IUGR or HELLP syndrome. The intensity of the Nix staining showed a similar pattern. In the syncytiotrophoblast, there was a weak bnip3 staining observable in the control as well as IUGR samples, whereas bnip3 was undetectable in preeclamptic placentas or those with HELLP syndrome. For Nix, only in the preeclampsia a weak staining was detectable, whereas all other probes were negative. Conclusions: Our study shows for the first time that the pro-apoptotic proteins bnip3 and Nix are expressed in the human placenta. Pregnancies with placental dysfunction and hypertensive pregnancy disorders with different clinical manifestations are characterized by a significantly decreased expression of bnip3 and Nix. These results suggest that the hypothesis of generally increased placental apoptosis in pregnancy-induced hypertensive disorders caused by disturbed trophoblast invasion has to be partly reconsidered. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

关键词： apoptosis preeclampsia bnip3 HELLP syndrome intrauterine growth retardation

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Mutagenesis data in the automated prediction of transmembrane helix dimers

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PROTEINS-STRUCTURE FUNCTION AND BIOINFORMATICS 2007年第2期67卷 375-384页

作者： Metcalf, Douglas G. Law, Peter B. DeGrado, William F. Univ Penn Sch Med Dept Biochem & Biophys Philadelphia PA 19104 USA

We present a molecular modeling protocol that selects modeled protein structures based on experimental mutagenesis results. The computed effect of a point mutation should be consistent with its experimental effect for correct models;mutations that do not affect protein stability and function should not affect the computed energy of a correct model while destabilizing mutations should have unfavorable computed energies. On the other hand, an incorrect model will likely display computed energies that are inconsistent with experimental results. We added terms to our energy function which penalize models that are inconsistent with experimental results. This creates a selective advantage for models that are consistent with experimental results in the Monte Carlo simulated annealing protocol we use to search conformational space. We calibrated our protocol to predict the structure of transmembrane helix dimers using glycophorin A as a model system. Inclusion of mutational data in this protocol compensates for the limitations of our force field and the limitations of our conformational. search. We demonstrate an application of this structure prediction protocol by modeling the transmembrane region of the bnip3 apoptosis factor.

关键词： Monte Carlo simulated annealing membrane protein transmembrane helix glycophorin A bnip3

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Split-ubiquitin膜蛋白酵母双杂交系统的构建及其应用

Split-ubiquitin膜蛋白酵母双杂交系统的构建及其应用

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作者：曹炜复旦大学

学位级别：博士

膜蛋白在生物体内参与了许多非常重要的过程,涉及物质运输,细胞的存活、增殖、分化,形态的发生与器官的形成等等各种信号的通路。对膜蛋白功能的研究一直都是比较活跃的领域。鉴于所发挥的重要功能,膜蛋白还被认为在疾病的诊断和治疗上... 详细信息

膜蛋白在生物体内参与了许多非常重要的过程,涉及物质运输,细胞的存活、增殖、分化,形态的发生与器官的形成等等各种信号的通路。对膜蛋白功能的研究一直都是比较活跃的领域。鉴于所发挥的重要功能,膜蛋白还被认为在疾病的诊断和治疗上都具有重要的地位。因此研究各种膜蛋白的功能对于阐明生物活动的规律是十分必要的。蛋白质总是通过和其它的蛋白或核酸相互作用而参与了细胞中的各种生命活动。以转录因子重构为基础的酵母双杂交是研究蛋白之间相互作用的非常有效的遗传学方法,并在功能蛋白质组研究中得到了广泛应用。但这种方法是将被研究的蛋白强制性地定位于细胞核内,不适合膜蛋白的研究。基于断裂泛素重组(split-ubiquitin)的酵母双杂交方法就是为满足膜蛋白研究的需要应运而生的,更适宜于研究膜蛋白-膜蛋白、膜蛋白-可溶性蛋白之间的相互作用。为方便研究膜蛋白之间或膜蛋白-可溶蛋白之间的相互作用,本课题的研究工作构建了一套split-ubiquitin膜蛋白酵母双杂交系统,为膜蛋白的研究提供了一个有效的平台。 Split-ubiquitin酵母双杂交方法的原理是利用连接有泛素(ubiquitin)的蛋白能够被泛素特异性的蛋白酶(UBPs)识别并切割下泛素,而这种特异性切割只在泛素能够正确折叠的前提下发生。在正常情况下,泛素断裂成两部分后在体内能自发结合成可被UBPs识别的重构泛素,而当有突变发生时,即泛素的N端发生Ile13/Gly13的突变,这种断裂泛素的重构就无法进行。只有当与断裂的泛素的两部分分别连接一个蛋白,且两个蛋白之间存在相互作用,断裂泛素的重组又得以恢复。断裂泛素重组的发生能将连接在泛素C端的转录因子切割并进入细胞核内激活报告基因的转录表达,通过报告基因是否表达,可以检测两个蛋白之间是否存在相互作用。根据这一原理,本研究课题构建了一套基于断裂泛素重组(split-ubiquitin)的酵母双杂交系统,并经过LASS2和VPL,一对能相互作用的人的膜蛋白的验证,可用于筛选膜蛋白相互作用的蛋白质。系统主要包括了含泛素C端部分(Cub)的pBait质粒,可克隆bait蛋白;含泛素N端部分(NubG)的pPrey质粒,可构建cDNA文库;含完整泛素(ubiquitin)的阳性对照质粒,可作为双杂交筛选时报告基因表达的阳性对照。与其它实验室已报道过的系统相比较,本系统的特点是:pBait和pPrcy质粒都是强启动子(ADH1和GAL1)、高拷贝数载体,相对地提高了相互作用蛋白的表达量,对于筛选较弱的相互作用具有一定的优势;pPrey质粒选用的诱导型启动子GAL1,使得prey蛋白的表达可受诱导物半乳糖的调控,能筛选对细胞有潜在毒性作用的蛋白。为验证新构建的split-ubiquitin酵母双杂交系统的有效性和实用性,本课题还分别以线粒体膜蛋白bnip3和结核杆菌胞壁蛋白Wag31为诱饵蛋白,利用这套系统筛选了与它们相互作用的蛋白,研究了bnip3在凋亡中的作用,探讨了Wag31在结核杆菌致病中的作用。 bnip3,是Bcl-2家族中含有单一BH3 domain的亚家族中一个成员,具有促细胞凋亡的功能。但同亚家族中的其它成员相比,bnip3有其独特之处,其所诱导的凋亡不依赖于caspase的激活和细胞色素c的释放,并造成线粒体功能的破坏。而且bnip3可能还参与了细胞自吞过程。但具体的过程并不十分清楚。bnip3的C端含有一段跨膜区将其定位在线粒体膜上发挥功能。利用本课题构建的膜蛋白酵母双杂交系统筛选到ACAA2,Acetyl-Coenzyme A acyltransferase 2,是bnip3相互作用的蛋白,能够减弱bnip3在HepG2和U-2 OS细胞中诱导的凋亡和对线粒体功能的破坏。这对深入理解bnip3的功能提供了新的证据,并在凋亡和脂肪酸代谢之间建立了可能的联系。这套系统的另一个应用是研究结核杆菌的致病机制。随着结核病的卷土重来,结核杆菌对人类健康的威胁越来越大,每年死于结核病的人已达200万。但对这种病原菌的致病机制的了解还非常有限。Wag31(Rv2145c)最初是从麻风病和结核病人的血清中作为致病的抗原被鉴定出的,这提示Wag31可能在结核杆菌的致病机制中发挥了重要作用,但像结核杆菌编码的很多蛋白一样,对其功能的研究还在初级阶段。以Wag31为bait,利用构建的系统首次发现趋化因子家族的成员之一XCL2能与Wag31发生相互作用,且Wag31能特异地激活XCL2在巨噬细胞中的表达。结果不仅把表达XCL2趋化因子的细胞类型扩大到巨噬细胞,还为阐明wag31和XCL2的生理和病理的重要性提供了新的思路。

关键词： split-ubiquitin 酵母双杂交 bnip3 结核杆菌 Wag31 趋化因子 XCL2

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探讨bnip3在利用维生素甲酸诱导U937细胞分化中所扮演的角色

探讨BNip3在利用维生素甲酸诱导U937细胞分化中所扮演的角色

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作者：汤永城中山医学大学

学位级别：硕士

急性前骨髓性白血病，是一种造血组织的恶性疾病，其治病原因乃骨髓性前趋细胞不正常的大量增生，并有细胞分化停止的病变。在之前的实验利用刘氏染色、cDNA microarry、RT-PCR、NBT还原实验、流式细胞仪、西方墨点法等实验得知，全反... 详细信息

急性前骨髓性白血病，是一种造血组织的恶性疾病，其治病原因乃骨髓性前趋细胞不正常的大量增生，并有细胞分化停止的病变。在之前的实验利用刘氏染色、cDNA microarry、RT-PCR、NBT还原实验、流式细胞仪、西方墨点法等实验得知，全反式维生素甲酸 (all-trans retinoic acid)诱导U937细胞分化成巨噬细胞时，bnip3蛋白质的表现量明显增加，而且把bnip3 antisense送入细胞中以RT-PCR与NBT还原实验等证实抑制bnip3蛋白质的表现会造成细胞分化的停止，但经由流式细胞仪侦测CD11b的表现量结果不具一致性，所以我们必须确认抑制bnip3蛋白质的表现时是否真的会造成细胞分化能力下降或当bnip3蛋白质的表现上升时是否会促进细胞的分化。本研究利用电穿孔（electroporation）的方式把bnip3 antisense或bnip3表现的载体（bnip3 expression vector）送入细胞内，借由流式细胞仪侦测细胞表面CD11b的表现量与西方墨点法侦测bnip3蛋白质的表现，结果显示出bnip3 antisense会抑制全反式维生素甲酸诱导U937细胞分化，与当送入bnip3表现的载体表达bnip3蛋白质时会造成细胞分化。此外我们为了了解在全反式维生素甲酸诱导U937细胞分化中有哪些转录因子在调控bnip3基因的表现，我们利用电穿孔的方式，将含有luciferase基因（reporter gene）的不同长度bnip3启动子载体转染（transfect）到U937细胞中，以观察在全反式维生素甲酸刺激下bnip3启动子的活性表现。结果显示以全反式维生素甲酸诱导U937细胞分化时，bnip3启动子 (promoter) 被两个转录因子所调控，其中MZF-1转录因子，其为bnip3 启动子的活化子 (activactor)，但我们利用gel retardation的方式，观察MZF-1转录因子与MZ-1探针结合的情形，没有明确的结果，有待进一步的实验探讨。另一个转录因子为AML-1α，其有可能为bnip3 启动子的抑制子 (repressor)，但也须进一步的实验确认。由我们的实验结果得到，当全反式维生素甲酸诱导U937细胞分化时会引起MZF-1与AML-1α转录因子产生，这两个转录因子调控bnip3的蛋白表现，以及bnip3蛋白的表现会诱导U937细胞分化。

关键词： bnip3 electroporation MZF-1 AML-1a

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BCL2 family of apoptosis-related genes: Functions and clinical implications in cancer

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CRITICAL REVIEWS IN CLINICAL LABORATORY SCIENCES 2006年第1期43卷 1-67页

作者： Thomadaki, H Scorilas, A Univ Athens Dept Biochem & Mol Biol Fac Biol Athens 15701 Greece

One of the most effective ways to combat different types of cancer is through early diagnosis and administration of effective treatment, followed by efficient monitoring that will allow physicians to detect relapsing disease and treat it at the earliest possible time. Apoptosis, a normal physiological form of cell death, is critically involved in the regulation of cellular homeostasis. Dysregulation of programmed cell death mechanisms plays an important role in the pathogenesis and progression of cancer as well as in the responses of tumours to therapeutic interventions. Many members of the BCL2 (B-cell CLL/lymphoma 2, Bcl-2)family of apoptosis-related genes have been found to be differentially expressed in various malignancies, and some are useful prognostic cancer biomarkers. We have recently cloned a new member of this family, BCL2L12, which was found to be differentially expressed in many tumours. Most of the BCL2 family genes have been found to play a central regulatory role in apoptosis induction. Results have made it clear that a number of coordinating alterations in the BCL2 family of genes must occur to inhibit apotosis and provoke carcinogenesis in a wide variety of cancers. However, more research is required to increase our understanding of the extent to which and the mechanisms by which they are involved in cancer development, providing the basis for earlier and more accurate cancer diagnosis, prognosis and therapeutic intervention that targets the apoptosis pathways. In the present review, we describe current knowledge of the function and molecular characteristics of a series of classic but also newly discovered genes of the BCL2 family as well as their implications in cancer development, prognosis and treatment.

关键词： apoptosis BCL2 gene family BCL-2 BCL2L12 cancer cancer prognosis cancer treatment tumour biomarkers BCL2L1 MCL1 BCL2L2 BOO/DIVA BCL2A1 BAX BAK1 BOK BIK BID HRK BCL2L11 bnip bnip1 bnip2 bnip3 NIX cebnip3 BLK PMAIP1 BMF BBC3 BCLAF1 BCL2L13 BCL2L14 MAP-1 BCL-B BCL2L10 BFK AIDS Alzheimer Parkinson spinal muscular atrophy Hashimoto thyroiditis glomerulonephritis Emery-Dreifuss muscular dystrophy

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Nitric oxide induces bnip3 expression that causes cell death in macrophages

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2004年第2期321卷 298-305页

作者： Yook, YH Kang, KH Maeng, O Kim, TR Lee, HO Kang, KI Kim, YS Paik, SG Lee, H Chungnam Natl Univ Dept Biol Taejon South Korea Chungnam Natl Univ Inst Biotechnol Taejon South Korea Korea Adv Inst Sci & Technol Dept Chem Taejon 305701 South Korea Chungnam Natl Univ Dept Biochem Taejon South Korea

Nitric oxide (NO) is involved in many physiological processes and also causes pathological effects by inducing apoptosis. It can enhance or suppress apoptosis depending on its concentration and the cell type involved. In this report, we used cDNA microarray analysis to show that SNAP, an NO donor, strongly induces Bcl-2/adenovirus EIB 19kDa-interacting protein 3 (bnip3) in macrophages. bnip3 is a mitochondrial pro-apoptotic protein that contains a Bcl-2 homology 3 domain and a COOH-terminal transmembrane (TM) domain. Macrophages activated by LPS/IFN-gamma produce nitric oxide synthase 2 (NOS2) and release endogenous NO. Expression of bnip3 was also induced in macrophages by LPS/IFN-gamma, and the induction was blocked by a NOS2 inhibitor, S-methyl-isothiourea. Peritoneal macrophages from NOS2-null mice failed to produce bnip3 in response to LPS/IFN-gamma. We conclude that bnip3 expression in macrophages is controlled by the intracellular level of nitric oxide. Overexpression of bnip3 but not of bnip3 DeltaTM, a bnip3 mutant without the TM domain and C-terminal tail, led to apoptosis of the cells. Promoter analysis showed that the region between -281 and -1 of the 5-upstream enhancer region of murine bnip3 was sufficient for NO-dependent expression of bnip3. (C) 2004 Elsevier Inc. All rights reserved.

关键词： apoptosis macrophage bnip3 nitric oxide

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Gene expression changes induced by bismuth in a macrophage cell line

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CELL AND TISSUE RESEARCH 2005年第2期321卷 195-210页

作者： Magnusson, NE Larsen, A Rungby, J Kruhoffer, M Orntoft, TF Stoltenberg, M Aarhus Univ Hosp Dept Endocrinol C DK-8000 Aarhus Denmark Aarhus Univ Hosp Dept Clin Biochem Mol Diagnost Lab DK-8000 Aarhus Denmark Univ Aarhus Inst Anat Dept Neurobiol Aarhus Denmark Univ Aarhus Dept Pharmacol DK-8000 Aarhus Denmark

We have investigated the effect of bismuth by autometallography, cell viability, TUNEL assay and microarray analysis of a macrophage cell line. The cells accumulate bismuth in their lysosomes in a time- and dose-dependent manner. Cell viability assays show a significant decrease in the number of viable cells related to both bismuth concentrations and exposure time. TUNEL assays after 12 h and 24 h at a bismuth-citrate concentration of 50 mu M revealed the presence of 30% and 70% TUNEL-positive cells, respectively, compared with 8% in the controls. We have analysed gene expression profiles for cells exposed to 50 mu M bismuth-citrate and for untreated controls at 12 h and 24 h by microarray analysis, which confirmed that bismuth is a powerful metallothionein inducer. A number of glycolytic enzymes are induced by bismuth, suggesting that bismuth is able to induce "hypoxia-like" stress. BCL2/adenovirus E1B 19-kDa-interacting protein 3 (bnip3) has been suggested as a regulator of hypoxia-induced cell death independent of caspase-3 activation and cytochrome c release. bnip3 is up-regulated indicating the involvement of bnip3 as a possible mechanism for bismuth-induced cell death. Differences have been noticed in cell viability and in the modification of the mRNA expression levels at 12 and 24 h. Only 13 genes are modified at both these times, suggesting a time-dependent molecular cascade in which bismuth-exposed cells enter a dormant stage with mRNA down-regulation being followed by cell death of susceptible cells.

关键词： heavy metals autometallography cell death microarray apoptosis bnip3 CRL-2192 cells (rat alveolar macrophage cell line)

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Functional characterization of human proapoptotic molecules in yeast S-cerevisiae

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FASEB JOURNAL 2005年第1期19卷 464-+页

作者： Guscetti, F Nath, N Denko, N Stanford Univ Sch Med Dept Radiat Oncol Div Radiat & Canc Biol Stanford CA 94305 USA

The presence of a complete (BH1-3) proapoptotic molecule is necessary for the induction of the intrinsic apoptotic cascade in mammalian cells. It is unclear, however, what distinct roles the members of the large family of BH3-only proapoptotic molecules play in apoptosis. Although biochemical analysis of these molecules can characterize binding efficiencies of BH3 family members, the biologic consequences of these interactions are difficult to predict. We have, therefore, established three functional categories of BH3-only human proapoptotic proteins based on their toxicity after expression in budding yeast: directly killing (tBid), sensitizing in Bax/Bcl-2 expressing cells ( Bad or Puma), and non-toxic (bnip3, bnip3L, and Noxa). The mechanism of killing by the proapoptotic molecules in yeast, however, is not due to activation of the recently described yeast metacaspase MCA1.

关键词： Bcl-2 Bax Bid Bad bnip3 bnip3L Noxa Puma metacaspase

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