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检索条件"主题词=Bnip3"

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Mechanisms of hyperbaric oxygen-induced neuroprotection in a rat model of subarachnoid hemorrhage

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM 2005年第5期25卷 554-571页

作者： Ostrowski, RP Colohan, ART Zhang, JH Loma Linda Univ Div Neurosurg Ctr Med Loma Linda CA 92350 USA Loma Linda Univ Dept Physiol Loma Linda CA 92350 USA

Acute cerebral ischemia occurs after subarachnoid hemorrhage (SAH) because of increased intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP). The effect of hyperbaric oxygen (HBO) on physiologic... 详细信息

Acute cerebral ischemia occurs after subarachnoid hemorrhage (SAH) because of increased intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP). The effect of hyperbaric oxygen (HBO) on physiological and clinical outcomes after SAH, as well as the expressions of hypoxia-inducible factor-1 alpha (HIF-1 alpha) and its target genes, such as bnip3 and VEGF was evaluated. Eighty-five male SD rats (300 to 350g) were randomly assigned to sham, SAH, and SAH + HBO groups. Subarachnoid hemorrhage was induced by endovascular perforation. Cortical cerebral blood flow (CBF), ICP, brain water content, brain swelling, neurologic function, and mortality were assessed. HBO (100% O-2, 2.8 ATA for 2 h) was initiated at 1 h after SAH. Rats were sacrificed at 24h to harvest tissues for Western blot or for histology. Apoptotic morphology accompanied by strong immunostaining of HIF-1 alpha, VEGF, and bnip3 were observed in the hippocampus and the cortex after SAH. Increased expressions of HIF-1 alpha, VEGF, and bnip3 were quantified by Western blot. HBO reduced the expressions of HIF-1 alpha, VEGF, and bnip3, diminished neuronal damage and improved CBF and neurologic function. HBO reduced early brain injury after SAH, probably by inhibition of HIF-1 alpha and its target genes, which led to the decrease of apoptosis and preservation of the blood-brain barrier function.

关键词： bnip3 early brain injury HBO HIF-1 alpha SAH VEGF

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bnip3 plays a role in hypoxic cell death in human epithelial cells that is inhibited by growth factors EGF and IGF

ONCOGENE 2003年第30期22卷 4734-4744页

作者： Kothari, S Cizeau, J McMillan-Ward, E Israels, SJ Bailes, M Ens, K Kirshenbaum, LA Gibson, SB Univ Manitoba Manitoba Inst Cell Biol Winnipeg MB Canada St Boniface Gen Hosp Res Ctr Inst Cardiovasc Sci Winnipeg MB R2H 2A6 Canada Univ Manitoba Fac Med Dept Physiol Winnipeg MB Canada Univ Manitoba Fac Med Dept Biochem & Med Genet Winnipeg MB Canada

Hypoxic regions within solid tumors are often resistant to chemotherapy and radiation. bnip3 (Bcl-2/E1B 19 kDa interacting protein) is a proapoptotic member of the Bcl-2 family that is expressed in hypoxic regions of ... 详细信息

Hypoxic regions within solid tumors are often resistant to chemotherapy and radiation. bnip3 (Bcl-2/E1B 19 kDa interacting protein) is a proapoptotic member of the Bcl-2 family that is expressed in hypoxic regions of tumors. During hypoxia, bnip3 expression is increased in many cell types and upon forced overexpression bnip3 induces cell death. Herein, we have demonstrated that blockage of hypoxia-induced bnip3 expression using antisense oligonucleotides against bnip3 or blockage of bnip3 function through expression of a mutant form of bnip3 inhibits hypoxia-induced cell death in human embryonic kidney 293 cells. We have also determined that hypoxia-mediated bnip3 expression is regulated by the transcription factor, hypoxia-inducible factor-1alpha (HIF-1alpha) in human epithelial cell lines. Furthermore, HIF-1alpha directly binds to a consensus HIF-1alpha-responsive element (HRE) in the human bnip3 promoter that upon mutation of this HRE site eliminates the hypoxic responsiveness of the promoter. Since bnip3 is expressed in hypoxic regions of tumors but fails to induce cell death, we determined whether growth factors block bnip3-induced cell death. Treatment of the breast cancer cell line MCF-7 cells with epidermal growth factor (EGF) or insulin-like growth factor effectively protected these cells from bnip3-induced cell death. Furthermore, inhibiting EGF receptor signaling using antibodies against ErbB2 (Herceptin) resulted in increased hypoxia-induced cell death in MCF-7 cells. Taken together, bnip3 plays a role in hypoxia-induced cell death in human epithelial cells that could be circumvented by growth factor signaling.

关键词： hypoxia cell death tumor bnip3 EGF IGF

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Expression of the cell death genes bnip3 and NIX in ductal carcinoma in situ of the breast;: correlation of bnip3 levels with necrosis and grade

JOURNAL OF PATHOLOGY 2003年第4期201卷 573-580页

作者： Sowter, HM Ferguson, M Pym, C Watson, P Fox, SB Han, C Harris, AL John Radcliffe Hosp Inst Mol Med Oxford OX3 9DS England John Radcliffe Hosp Nuffield Dept Clin Lab Sci Oxford England John Radcliffe Hosp Dept Histopathol Oxford OX3 9DU England Univ Manitoba Winnipeg MB R3E 0W3 Canada Churchill Hosp Dept Stat Oxford OX3 7LJ England

Ductal carcinoma in situ (DCIS) of the breast is an early, non-invasive lesion and the prognosis is associated with the extent of necrosis and cell death within the tumour. Two cell death genes, bnip3 and NIX, are up-... 详细信息

Ductal carcinoma in situ (DCIS) of the breast is an early, non-invasive lesion and the prognosis is associated with the extent of necrosis and cell death within the tumour. Two cell death genes, bnip3 and NIX, are up-regulated in response to hypoxia in breast carcinoma cells, although any involvement of either gene in disease progression is currently unknown. This study has analysed the expression of bnip3 and NIX in 56 samples of breast DCIS, as well as in adjacent benign and invasive breast tissue. Both genes are strongly expressed in the epithelial component of a subset of DCIS and invasive disease. The data show a correlation between high expression of bnip3 in the DCIS cells and a high-grade, necrotic lesion that is likely to be associated with invasive tumour. bnip3 was present in tumour-associated macrophages and in apocrine metaplastic lesions. Expression of NIX did not correlate with any of the parameters investigated Copyright (C) 2003 John Wiley Sons, Ltd.

关键词： bnip3 hypoxia ductal carcinoma in situ of the breast necrosis cell death

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转移能力不同的肺癌细胞中p53基因相关凋亡调控通路的功能研究

转移能力不同的肺癌细胞中p53基因相关凋亡调控通路的功能研究

作者：金焰哈尔滨医科大学

学位级别：博士

p53基因是重要的抑癌基因之一。它抑制肿瘤细胞增殖、参与细胞凋亡、分化、修复等生命活动。本研究室的前期研究结果表明，以腺病毒为载体的野生型p53基因(Ad-p53)可介导肺癌细胞发生凋亡。\n 为探讨该作用的机理，本研究选择了两对来... 详细信息

p53基因是重要的抑癌基因之一。它抑制肿瘤细胞增殖、参与细胞凋亡、分化、修复等生命活动。本研究室的前期研究结果表明，以腺病毒为载体的野生型p53基因(Ad-p53)可介导肺癌细胞发生凋亡。\n 为探讨该作用的机理，本研究选择了两对来源相同，转移能力不同的肺癌细胞系(人肺腺癌细胞系：AGZY83-a和Anip973；人巨细胞肺癌细胞系：95C和95D)，其中AGZY83-a和95C为低转移细胞系，Anip973和95D为高转移细胞系，分别应用Ad-p53感染上述四种细胞系，结果均导致细胞凋亡，且高转移细胞系的凋亡速率要高于低转移细胞系。\n 为进一步探讨p53与bnip3的作用关系，收获了经Ad-p53感染后的Anip973细胞和转染bnip3后AGZY83-a细胞总蛋白，应用免疫共沉淀方法(Co-IP)分别检测p53与bnip3蛋白的表达。以p53抗体做IP，用bnip3抗体可以检测到bnip3的表达；反之，以bnip3抗体IP，用p53抗体也可以检测到p53的表达。表明p53与bnip3的关系密切，可能通过直接相互作用机制参与凋亡的进程。这可能也是p53介导高转移肺癌细胞系快速凋亡的机制之一。

关键词： p53 bnip3 肺癌细胞基因凋亡细胞增殖

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Hypoxia-inducible factors and hypoxic cell death in tumour physiology

ANNALS OF MEDICINE 2004年第7期36卷 530-539页

作者： Bacon, AL Harris, AL John Radcliffe Hosp Weatherall Inst Mol Med Canc Res UK Oxford OX3 9DU England

Hypoxic up-regulation of hypoxia-inducible factors (HIFs) during tumourigenesis presents an interesting paradox with respect to their role in tumour growth. Hypoxia-inducible factor I (HIF-1) plays a key role in the a... 详细信息

Hypoxic up-regulation of hypoxia-inducible factors (HIFs) during tumourigenesis presents an interesting paradox with respect to their role in tumour growth. Hypoxia-inducible factor I (HIF-1) plays a key role in the adaptive response to hypoxia, trans-activating many genes whose protein products are involved in pathways of angiogenesis, glucose metabolism and cell proliferation, thus facilitating tumour progression. However, it is also emerging that up-regulation of HIF-1 trans-activates anti-proliferative and pro-apoptotic genes (such as bnip3, NIX and IGFBP3). This makes it unclear as to whether HIF-1 up-regulation provides a selective advantage or disadvantage to neoplastic progression under hypoxia. In addition, vagaries in the hypoxic microenvironment of the tumour such as pH changes, presence of reactive oxygen species and energy availability in the form of adenosine triphosphate (ATP), appear to influence the function of HIF-1 and up-regulated pathways and affect susceptibility to undergo hypoxic cell death. It is apparent that hypoxic cancer cells must be able to select against HIF-1 mediated cell death signals in order to survive and progress towards malignancy. Hypoxia-induced HIF-1 may in itself serve to select for increased malignancy by exerting pressure in the form of anti-proliferative signals that must be escaped. Understanding the mechanisms by which HIF-1 induces cell death and the manner in which the tumour cell can overcome such signals, is critical for our understanding of cancer progression and the development of effective therapeutics.

关键词： apoptosis bnip3 hypoxia-inducible factor necrosis

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Modes of cell death in rat liver after monocrotaline exposure

TOXICOLOGICAL SCIENCES 2004年第1期77卷 172-182页

作者： Copple, BL Rondelli, CM Maddox, JF Hoglen, NC Ganey, PE Roth, RA Michigan State Univ Dept Pharmacol & Toxicol Inst Environm Toxicol E Lansing MI 48824 USA Michigan State Univ Natl Food Safety & Toxicol Ctr E Lansing MI 48824 USA IDUN Pharmaceut Inc San Diego CA 92121 USA

Monocrotaline (MCT) is a pyrrolizidine alkaloid (PA) plant toxin that produces sinusoidal endothelial cell (SEC) injury, hemorrhage, fibrin deposition, and coagulative hepatic parenchymal cell (HPC) oncosis in centril... 详细信息

Monocrotaline (MCT) is a pyrrolizidine alkaloid (PA) plant toxin that produces sinusoidal endothelial cell (SEC) injury, hemorrhage, fibrin deposition, and coagulative hepatic parenchymal cell (HPC) oncosis in centrilobular regions of rat livers. Cells with apoptotic morphology have been observed in the livers of animals exposed to other PAs. Whether apoptosis occurs in the livers of MCT-treated animals and whether it is required for full manifestation of pathological changes is not known. To determine this, rats were treated with 300 mg MCT/kg, and apoptosis was detected by transmission electron microscopy and the TUNEL (TdT-mediated dUTP nick end labeling) assay. MCT produced significant apoptosis in the liver by 4 h after treatment. To determine if MCT kills cultured HPCs by apoptosis, HPCs were isolated from the livers of rats and exposed to MCT. MCT caused a concentration-dependent release of alanine aminotransferase (ALT), a marker of HPC injury. Furthermore, caspase 3 was activated and TUNEL staining increased in MCT-treated HPCs. MCT-induced TUNEL staining and release of ALT into the medium were completely prevented by the pancaspase inhibitors *** and IDN-7314, suggesting that MCT kills cultured HPCs by apoptosis. To determine if caspase inhibition prevents MCT-induced apoptosis in the liver, rats were cotreated with MCT and IDN-7314. IDN-7314 reduced MCT-induced TUNEL staining in the liver and release of ALT into the plasma. Morphometric analysis confirmed that IDN-7314 reduced HPC oncosis in the liver by approximately 50%. Inasmuch as HPC hypoxia occurred in the livers of MCT-treated animals, upregulation of the hypoxia-regulated cell-death factor, bnip3 (Bcl2/adenovirus EIB 19kD-interacting protein 3), was examined. bnip3 was increased in the livers of mice treated 24 h earlier with MCT. Results from these studies show that MCT kills cultured HPCs by apoptosis but causes both oncosis and apoptosis in the liver in vivo. Furthermore, caspase inhibiti

关键词： monocrotaline liver rat apoptosis caspase 3 bnip3 hypoxia oncosis

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The role of hypoxia inducible factor 1α in cobalt chloride induced cell death in mouse embryonic fibroblasts

TOXICOLOGICAL SCIENCES 2004年第2期82卷 638-646页

作者： Vengellur, A LaPres, JJ Michigan State Univ Dept Biochem & Mol Biol E Lansing MI 48824 USA Michigan State Univ Grad Program Genet E Lansing MI 48824 USA Michigan State Univ Natl Food Safety & Toxicol Ctr E Lansing MI 48824 USA Michigan State Univ Ctr Integrat Toxicol E Lansing MI 48824 USA

Cobalt has been widely used in the treatment of anemia and as a hypoxia mimic in cell culture and it is known to activate hypoxic signaling by stabilizing the hypoxia inducible transcription factor 1alpha (HIF1alpha).... 详细信息

Cobalt has been widely used in the treatment of anemia and as a hypoxia mimic in cell culture and it is known to activate hypoxic signaling by stabilizing the hypoxia inducible transcription factor 1alpha (HIF1alpha). However, cobalt exposure can lead to tissue and cellular toxicity. These studies were conducted to determine the role of HIF1alpha in mediating cobalt-induced toxicity. Mouse embryonic fibroblasts (MEFs) that were null for the HIF1alpha protein were used to show that HIF1alpha protein plays a major role in mediating cobalt-induced cytotoxicity. Previous work from our lab and others has shown that two BH3 domain containing cell death genes, bnip3 and NIX, are targets of hypoxia signaling. These experiments document that bnip3 and NIX expression is HIF1alpha-dependent, and cobalt induces their expression in a time and dose dependent manner. In addition, their expression is correlated with an increase in bnip3 and NIX protein. Characteristically, the elevated level of bnip3 was correlated with an increased presence of chromatin condensation, one marker for cell injury. Interestingly, this increased chromosomal condensation was not coupled to caspase-3 activation as usually seen in a typical apoptotic response. These results show that HIF1alpha is playing a major role in mediating cobalt-induced toxicity in mouse embryonic fibroblasts and may offer a possible mechanism for the underlying pathology of injuries seen in workers exposed to environmental contaminants that can influence the hypoxia signaling system, such as cobalt.

关键词： cobalt hypoxia toxicity bnip3 metal

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The carboxy terminal c-tail of bnip3 is crucial in induction of mitochondrial permeability transition in isolated mitochondrial

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS 2002年第2期398卷 147-152页

作者： Kim, JY Cho, JJ Ha, J Park, JH Kyung Hee Univ Coll Med Dept Pathol Seoul 130701 South Korea Kyung Hee Univ Coll Med Dept Microbiol Seoul 130701 South Korea Kyung Hee Univ Coll Med Dept Mol Biol Seoul 130701 South Korea

bnip3 is a member of Bcl-2 family proteins that displays proapoptotic activity. It contains Bcl-2 homology (1311) 3 and single carboxy terminal membrane-anchoring domain (TM), which targets to specific intracellular o... 详细信息

bnip3 is a member of Bcl-2 family proteins that displays proapoptotic activity. It contains Bcl-2 homology (1311) 3 and single carboxy terminal membrane-anchoring domain (TM), which targets to specific intracellular organelles, especially to mitochondria. Mitochondria play significant roles in apoptosis by releasing apopto-genic factors through large conductance channel known as permeability transition pore (PTP). Although bnip3 associates with mitochondria when overexpressed, apoptotic pathways including mitochondrial cascade and functional domains of bnip3 are still unknown. in this report, we demonstrate that recombinant bnip3 (rbnip3) induces mitochondrial permeability transition (MPT) and cytochrome c release from isolated mitochondria, which are inhibited by the PT inhibitor cyclosporin A (CsA). We further show that carboxy terminal tail of bnip3, but not BH3, is essential for the induction of PT and cytochrome c release on the base of mutational analysis. Moreover, addition of carboxy terminal c-tail to TM substitution mutant, which did not induce the PT and cytochrome c release, restored PT-inducing activity. Taken together, our results suggest that bnip3 exerts proapoptotic activity through PT induction and that carboxy terminal c-tail is crucial for it. (C) 2002 Elsevier Science (USA).

关键词： bnip3 permeability transition BH3 transmembrane domain cytochrome c

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Nuclear export of adenovirus E4orf6 protein is necessary for its ability to antagonize apoptotic activity of BH3-only proteins

ONCOGENE 2003年第44期22卷 6919-6927页

作者： Aoyagi, M Higashino, F Yasuda, M Takahashi, A Sawada, Y Totsuka, Y Kohgo, T Sano, H Kobayashi, M Shindoh, M Hokkaido Univ Grad Sch Dent Med Dept Oral Pathobiol Sci Kita Ku Sapporo Hokkaido 0608586 Japan Hokkaido Univ Grad Sch Dent Med Dept Oral Hlth Sci Kita Ku Sapporo Hokkaido 0608586 Japan Hokkaido Inst Publ Hlth Dept Biol Sapporo Hokkaido 0600819 Japan Hokkaido Univ Sch Med Inst Med Genet Div Canc Pathobiol Sapporo Hokkaido 0608638 Japan

The adenovirus E4orf6 is a viral oncoprotein known to cooperate with the E1A gene product in transforming primary murine cells. It has been shown to inhibit the apoptotic activities of p53 and p73 through direct bindi... 详细信息

The adenovirus E4orf6 is a viral oncoprotein known to cooperate with the E1A gene product in transforming primary murine cells. It has been shown to inhibit the apoptotic activities of p53 and p73 through direct binding to these proteins. Here, we demonstrate that the adenovirus E4orf6 protein inhibits apoptosis mediated by bnip3 and Bik, which are BH3-only proteins of the Bcl-2 family. This activity was not mediated by p53 and p73 because E4orf6 had the same effect on the apoptosis in Saos-2 cells that do not express p53-related genes. It was also ascertained that E4orf6 could change the mitochondrial localization of bnip3 and Bik. A mutant lacking the nuclear export signal of E4orf6 failed to inhibit apoptosis and to translocate bnip3 protein from the mitochondria. Moreover, it was also established that E4orf6 was able to interact with bnip3 and Bik. In bnip3 protein, the region required for the interaction included the transmembrane domain, which is required for the localization of bnip3 to the mitochondria. These results suggest that E4orf6 is exported from the nucleus to the cytoplasm, enabling it to interact with BH3-only proteins, eventually leading to the inhibition of apoptotic activity.

关键词： E4orf6 adenovirus nuclear export BH-3 only protein bnip3 Bik

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Hypoxia induces the expression of the pro-apoptotic gene bnip3

CELL DEATH AND DIFFERENTIATION 2001年第4期8卷 367-376页

作者： Guo, K Searfoss, G Krolikowski, D Pagnoni, M Franks, C Clark, K Yu, KT Jaye, M Ivashchenko, Y AVENTIS PHARMA Cardiovasc Biol D-65926 Frankfurt Germany

It has been shown that oxygen deprivation results in apoptotic cell death, and that hypoxia inducible factor 1 (HIF1) and the tumor suppressor p53 play key roles in this process. However, the molecular mechanism throu... 详细信息

It has been shown that oxygen deprivation results in apoptotic cell death, and that hypoxia inducible factor 1 (HIF1) and the tumor suppressor p53 play key roles in this process. However, the molecular mechanism through which hypoxia and HIF1 induce apoptosis is not clear. Here we show that the expression of pro-apoptotic gene bnip3 is dramatically induced by hypoxia in various cell types, including primary rat neonatal cardiomyocytes. Overexpression of HIF1 alpha, but not p53, induces the expression of bnip3, Overexpression of bnip3 leads to a rather unusual type of apoptosis, as no cytochrome c leakage from mitochondria was detected and inhibitors of caspases were unable to prevent cell death. Taken together, these data suggest that HIF1-dependent induction of bnip3 may play a significant role during hypoxia-induced cell death.

关键词： bnip3 hypoxia cardiomyocytes apoptosis

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