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Evidence of oxidative stress-induced bnip3 expression in amyloid beta neurotoxicity

BRAIN RESEARCH 2007年第0期1138卷 221-230页

作者： Zhang, Surong Zhang, Zhengfeng Sandhu, Garry Ma, Xiuli Yang, Xuefen Geiger, Jonathan D. Kong, Jiming Univ Manitoba Fac Med Dept Human Anat & Cell Sci Winnipeg MB R3E 0W3 Canada Univ N Dakota Sch Med & Hlth Sci Dept Pharmacol Physiol & Therapeut Grand Forks ND 58203 USA

The formation of A beta and its subsequent deposition in senile plaques are considered to be initial events that lead to a cascade of pathological changes in AD. Mediators of A beta-induced oxidative stress are known to cause oxidative damage to macromolecules. However, the molecular mechanisms by which A beta-induced oxidative stress leads to neuronal cell death are not fully understood. Here we show that A beta-induced oxidative stress activates the prodeath gene bnip3. A beta treatment results in mitochondrial dysfunction, accumulation of reactive oxygen species, and subsequent expression of bnip3 in rat primary cortical neurons. Pretreatment with antioxidants abolished A beta-induced bnip3 expression and attenuated cell death, demonstrating the role of oxidative stress in bnip3 induction. A beta-induced bnip3 expression may be mediated by hypoxia-inducible factor-1 (HIF-1) because A beta-treatment induced accumulation and nuclear translocation of HIF-1 and knock-down of HIF-1 by RNAi inhibited bnip3 expression. Finally, knockdown of bnip3 reduced A beta-induced neuronal death. Together, these results suggest a potential pathological role of bnip3 in the etiology of AD. (c) 2007 Elsevier B.V. All rights reserved.

关键词： Alzheimer's disease amyloid beta bnip3 oxidative stress mitochondria neuron

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Platonin protects against cerebral ischemia/reperfusion injury in rats by inhibiting NLRP3 inflammasomes via bnip3/LC3 signaling mediated autophagy

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BRAIN RESEARCH BULLETIN 2022年第0期180卷 12-23页

作者： Luo, Jing Tan, Junyi Jiang, Ning Yang, Changhong Chen, Jialei Zhao, Jing Li, Lingyu Zhao, Yong Chongqing Med Univ Dept Pathol Chongqing 400016 Peoples R China Chongqing Med Univ Dept Pathophysiol Chongqing 400016 Peoples R China Chongqing Med Univ Dept Bioinformat Chongqing 400016 Peoples R China Chongqing Med Univ Inst Neurosci Chongqing 400016 Peoples R China

Studies have found that Platonin has neuroprotective effect, but its molecular mechanism needs further study. We found that at the early stage of cerebral ischemia/reperfusion injury, Platonin treatment significantly reduced cerebral infarct lesions, improved neurological scores, and exerted neuroprotective effects. Our group has shown that NLRP3 inflammasomes activation is required to mediate neuronal injury during cerebral ischemia /reperfusion injury. The brain protective effect of Platonin is related to its ability to effectively regulate autophagy and NLRP3 inflammasomes-derived inflammation. Platonin treatment effectively induced autophagy (LC3II/I, p62) and reduced NLRP3 inflammasomes activation(NLRP3, cleaved-IL-113,cleaved-IL-18, cleaved-caspase1). However, 3-MA (15 mg/kg) treatment downregulated the inhibitory effect of Platonin on NLRP3 inflammasomes. We also studied the location of bnip3 in Platonin-mediated neuroprotection and found that Platonin induced the expression of autophagic protein bnip3 and enhanced the co-immunoprecipitation of bnip3 with LC3, and double-labeled immunofluorescence also showed enhanced co-localization of bnip3 with LC3. Finally, si-bnip3 transfection attenuated the co localization of bnip3 with LC3, decreased the autophagy activity to a certain extent and blocked the inhibition of NLRP3 inflammasomes-derived inflammation by Platonin. This study demonstrated that Platonin may play a neuroprotection role in cerebral I / R injury by inhibiting NLRP3 inflammasomes activation through upregulating autophagy via bnip3 / LC3 pathway.

关键词： Platonin bnip3 LC3 Autophagy NLRP3 inflammasomes Inflammation Neuroprotection Cerebral I R injury

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Autophagy and Bcl-2/bnip3 death regulatory pathway in non-small cell lung carcinomas

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APMIS 2013年第7期121卷 592-604页

作者： Karpathiou, Georgia Sivridis, Efthimios Koukourakis, Michael Mikroulis, Dimitrios Bouros, Demosthenes Froudarakis, Marios Bougioukas, George Maltezos, Efstratios Giatromanolaki, Alexandra Democritus Univ Thrace Dept Pathol Sch Med Alexandroupolis 68100 Greece Democritus Univ Thrace Dept Radiotherapy Oncol Sch Med Alexandroupolis 68100 Greece Democritus Univ Thrace Dept Cardiac Thorac Surg Sch Med Alexandroupolis 68100 Greece Democritus Univ Thrace Dept Pneumonol Sch Med Alexandroupolis 68100 Greece Democritus Univ Thrace Dept Internal Med Sch Med Alexandroupolis 68100 Greece

We recently showed that non-small cell lung carcinomas (NSCLCs) are of dismal prognosis when encompassing accelerated autophagic activity. The regulation of this abnormally functioning degradation system and its association with hypoxia and apoptosis in lung carcinoma patients is unexplored. In this study we used 115 NSCLC tissues to examine the immunohistochemical expression of four distinct molecules - the major regulator of autophagy Beclin 1, the anti-apoptotic and anti-autophagic protein Bcl-2, the pro-apoptotic and pro-autophagic protein bnip3, and a marker of hypoxia and glucolysis, the glucose transporter Glut 1. Most cases showed reduced reactivity for Beclin 1 (62%) and Bcl-2 (82%) proteins, almost half of our sample revealed strong bnip3 expression (57%), whereas most of the carcinomas strongly expressed Glut 1 antigen (71%). Beclin 1 expression showed no association with survival. Bcl-2 positivity was a marker of good prognosis (p=0.04), whereas bnip3 (p=0.0004) and Glut 1 (p=0.03) expression correlated with poor outcome in Stage I disease. Autophagic status was negatively associated with Bcl-2 (p=0.0006), but positively with Glut 1 expression (p=0.001). In conclusion, the accelerated autophagic status in NSCLC is unrelated to Beclin 1 and bnip3 expression, but does show significant association with Bcl-2 reactivity. Furthermore, we showed important correlations between glucolysis and autophagy, guiding new pathways in future lung carcinoma research.

关键词： Autophagy apoptosis glycolysis hypoxia LC3A bnip3 Beclin 1 Bcl-2 Glut 1 lung caner prognosis biology immunohistochemistry

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Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (bnip3) expression is epigenetically regulated by one-carbon metabolism in invasive duct cell carcinoma of breast

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MOLECULAR AND CELLULAR BIOCHEMISTRY 2012年第1-2期361卷 189-195页

作者： Naushad, Shaik Mohammad Prayaga, Aruna Digumarti, Raghunadha Rao Gottumukkala, Suryanarayana Raju Kutala, Vijay Kumar Nizams Inst Med Sci Dept Clin Pharmacol & Therapeut Hyderabad 500082 Andhra Pradesh India Nizams Inst Med Sci Dept Pathol Hyderabad 500082 Andhra Pradesh India Nizams Inst Med Sci Dept Med Oncol Hyderabad 500082 Andhra Pradesh India Nizams Inst Med Sci Dept Surg Oncol Hyderabad 500082 Andhra Pradesh India

In view of recent studies highlighting the prognostic relevance of expression and CpG island methylator phenotype (CIMP) of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (bnip3) in invasive duct cell carcinoma (IDC), we hypothesized in this article that impaired one-carbon metabolism might influence CIMP phenotype of bnip3. In order to substantiate the prognostic relevance of bnip3, we explored its association with 8-oxo-2'deoxyguanosine (8-oxodG), a marker of oxidative stress with prognostic relevance. bnip3 expression and CIMP phenotype were studied using semi-quantitative RT-PCR and combined bisulfite restriction analysis (COBRA), respectively, in 56 IDC tumors. Eight polymorphisms in one-carbon metabolism were studied using PCR-RFLP and PCR-AFLP approaches. 8-oxodG was measured using competitive ELISA kit. bnip3 was found to be upregulated in IDC (cases vs. controls: 0.94 +/- A 0.05 vs. 0.18 +/- A 0.08, P < 0.0001). COBRA analysis confirmed hypomethylation of bnip3 promoter CpG island in these cases. CIMP phenotype of bnip3 showed positive association with tubule formation (P = 0.034) and methionine synthase reductase (MTRR) A66G (P = 0.002);inverse association with cytosolic serine hydroxyl methyltransferase (cSHMT) C1420T (P < 0.005) and 8-oxodG (< 10% vs. > 10% methylation: 7.24 +/- A 2.77 ng/ml vs. 4.42 +/- A 2.93 ng/ml, P < 0.0005);and no association with nuclear pleomorphism or mitotic index or ER, PR, and HER statuses. Synergistic effect of MTR A2756G and MTRR A66G variants on bnip3 hypermethylator phenotype was clearly evident (P < 0.0007). MTRR A66G and cSHMT C1420T polymorphisms influence CIMP phenotype of bnip3, thus epigenetically regulating bnip3 in breast cancer. The linear association between bnip3 and 8-oxodG substantiates the role of bnip3 as redox sensor as well as prognostic marker in breast cancer.

关键词： bnip3 One-carbon metabolism CpG island methylator phenotype 8-Oxo-2 '-deoxyguanosine

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Poorer outcome in stromal HIF-2α- and CA9-positive colorectal adenocarcinomas is associated with wild-type TP53 but not with bnip3 promoter hypermethylation or apoptosis

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BRITISH JOURNAL OF CANCER 2008年第5期99卷 727-733页

作者： Cleven, A. H. G. Wouters, B. G. Schutte, B. Spiertz, A. J. G. van Engeland, M. de Bruine, A. P. Univ Hosp Dept Pathol GROW Sch Oncol & Dev Biol NL-6202 AZ Maastricht Netherlands Ontario Canc Inst PMH Toronto ON M4X 1K9 Canada Univ Hosp Dept Mol Cell Biol GROW Sch Oncol & Dev Biol NL-6202 AZ Maastricht Netherlands

Stromal expression of hypoxia inducible factor 2 alpha (HIF-2 alpha) and carbonic anhydrase 9 (CA9) are associated with a poorer prognosis in colorectal cancer (CRC). Tumour cell death, regulated by a hypoxic stromal microenvironment, could be of importance in this respect. Therefore, we correlated apoptosis, TP53 mutational status and bnip3 promoter hypermethylation of CRC cells with HIF-2 alpha- and CA9-related poor outcome. In a series of 195 CRCs, TP53 mutations in exons 5-8 were analysed by direct sequencing, and promoter hypermethylation of bnip3 was determined by methylation-specific PCR. Expressions of HIF-2 alpha, CA9, p53, bnip3 and M30 were analysed immunohistochemically. Poorer survival of HIF-2 alpha and CA9 stromal-positive CRCs was associated with wild-type TP53 ( P = 0.001 and P = 0.0391), but not with bnip3 methylation. Furthermore, apoptotic levels were independent of the TP53 status, but lower in unmethylated bnip3 CRCs ( P = 0.004). It appears that wild-type TP53 in CRC cells favours the progression of tumours expressing markers for hypoxia in their stroma, rather than in the epithelial compartment. Preserved bnip3 function in CRC cells lowers apoptosis, and may thus be involved in alternative cell death pathways, such as autophagic cell death. However, bnip3 silencing in tumour cells does not impact on hypoxia-driven poorer prognosis. These results suggest that the biology of CRC cells can be modified by alterations in the tumour microenvironment under conditions of tumour hypoxia.

关键词： colorectal cancer hypoxia TP53 bnip3 outcome

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HIF-1α activation by a redox-sensitive pathway mediates cyanide-induced bnip3 upregulation and mitochondrial-dependent cell death

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FREE RADICAL BIOLOGY AND MEDICINE 2007年第1期43卷 117-127页

作者： Zhang, L. Li, L. Liu, H. Prabhakaran, K. Zhang, X. Borowitz, J. L. Isom, G. E. Purdue Univ Dept Med Chem & Mol Pharmacol W Lafayette IN 47907 USA

Cyanide produces degeneration of the nervous system in which different modes of cell death are activated in the vulnerable brain areas. In brain, the mechanism underlying the cell death is not clear. In this study, an immortalized dopaminergic cell line was used to characterize the cell death signaling cascade activated by cyanide. Cyanide-treated cells exhibited a time- and concentration-dependent apoptosis that was caspase independent. Cyanide induced a rapid surge of intracellular reactive oxygen species (ROS) generation, followed by p38 mitogen-activated protein kinase (MAPK) activation and nuclear accumulation of hypoxia-inducible factor-1 alpha (HIF-1 alpha). Activation of p38 MAPK and HIF-1 alpha accumulation were attenuated by N-acetyl-L-cysteine (antioxidant), catalase (hydrogen peroxide scavenger), or a selective p38 MAPK inhibitor (SB203580). Cyanide activated the hypoxia response element (HRE) promoter, which was also blocked by the antioxidants and SB203580. HRE activation was followed by increased bnip3 gene transcription, as reflected by elevated bnip3 mRNA and protein levels. bnip3 upregulation was reduced by selective RNAi knockdown of HIF-1 alpha. Overexpression of bnip3 produced mitochondrial dysfunction (reduced membrane potential), caspase-independent apoptosis, and sensitization of the cells to cyanide-induced toxicity. Expression of a dominant-negative mutant or RNAi knockdown of bnip3 protected the cells from cyanide. It was concluded that cyanide activated the HIF-1 alpha-mediated pathway of bnip3 induction through a redox-sensitive process. Increased bnip3 expression then served as an initiator of mitochondrial-mediated death. (c) 2007 Elsevier Inc. All rights reserved.

关键词： cyanide HIF-1 alpha bnip3 cell death reactive oxygen species RNA interference

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Synergism of arsenic trioxide and MG132 in Raji cells attained by targeting bnip3, autophagy, and mitochondria with low doses of valproic acid and vincristine

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EUROPEAN JOURNAL OF CANCER 2014年第18期50卷 3243-3261页

作者： Cavaliere, Victoria Lombardo, Tomas Costantino, Susana N. Kornblihtt, Laura Alvarez, Elida M. Blanco, Guillermo A. UBA IDEHU CONICET Lab Inmunotoxicol LaITo Hosp Clin RA-1113 Buenos Aires DF Argentina UBA Fac Farm & Bioquim IDEHU CONICET LIT RA-1113 Buenos Aires DF Argentina UBA Hosp Clin Serv Hematol RA-1113 Buenos Aires DF Argentina

We previously demonstrated that arsenic trioxide (ATO) and proteasome inhibitor MG132 synergistically induced cell death in promonocytic leukaemia cell line U937 but were antagonistic in Burkitt's lymphoma cell line Raji. Here we explore the role of autophagy, expression of bnip3, and mitochondrial mass, in determining whether ATO and MG132 interaction can be shifted from antagonism to synergism in Raji cells. Treatment with ATO + MG132 increased the percentage of cells with collapsed mitochondrial membrane potential (MMP) in U937 cells, but had no effect in Raji cells. Mitochondria were found in cytoplasmic marginal location in U937 cells but at perinuclear location in Raji cells. ATO + MG132 increased mitochondrial mass in U937 cells but decreased it in Raji cells, while autophagy was increased in both cell lines. bnip3 was expressed in U937 cells at cytoplasmic marginal locations and was hardly detected in Raji cells. Histone deacetylase (HDAC) inhibitor valproic acid (VPA) increased expression of bnip3 in Raji cells at perinuclear locations. However antagonism between ATO and MG132 was increased in the presence of low doses of VPA. Addition of vincristine (VCR) blocked autophagy, while VPA + VCR treatment of Raji cells at sub-cytotoxic doses caused bnip3 and mitochondria to redistribute to cytoplasmic peripheral location and increased mitochondrial mass. ATO + MG132 in the presence of subcytotoxic doses of VPA + VCR caused collapse of MMP in Raji cells, while interaction between ATO and MG132 shifted from antagonism to synergism. We conclude that synergism between ATO and MG132 was attained in Raji cells by disruption of the perinuclear mitochondrial cluster, blockage of selective autophagy of mitochondria (mitophagy) by VCR, increased mitochondrial mass, and upregulation of bnip3 by VPA. (C) 2014 Elsevier Ltd. All rights reserved.

关键词： Synergism bnip3 Mitochondria Mitophagy Autophagy Targeted combined therapies Arsenic trioxide MG132 Valproic acid Burkitt's lymphoma

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Semaglutide attenuates doxorubicin-induced cardiotoxicity by ameliorating bnip3-Mediated mitochondrial dysfunction

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REDOX BIOLOGY 2024年 72卷 103129页

作者： Li, Xiaoping Luo, Wenbin Tang, Yang Wu, Jiangjiao Zhang, Junkai Chen, Shengnan Zhou, Lu Tao, Yu Tang, Yuanjuan Wang, Fengxian Huang, Yu Jose, Pedro A. Guo, Li Zeng, Chunyu Third Mil Med Univ Army Med Univ Daping Hosp Dept Cardiol Chongqing Peoples R China Chongqing Inst Cardiol Chongqing Cardiovasc Clin Res Ctr Key Lab Geriatr Cardiovasc & Cerebrovasc Dis Res Chongqing Key Lab Hypertens ResMinist Educ China Chongqing Peoples R China Chongqing Univ Coll Bioengn Chongqing Peoples R China Southwest Jiaotong Univ Peoples Hosp Hosp Chengdu 3 Dept Cardiol Affiliated Hosp Chengdu Peoples R China City Univ Hong Kong Dept Biomed Sci Hong Kong Peoples R China George Washington Univ Div Renal Dis & Hypertens Sch Med & Hlth Sci Washington DC USA Army Med Univ Mil Med Univ 3 Endocrinol Dept Affiliated Hosp 1 Chongqing Peoples R China Third Mil Med Univ Daping Hosp State Key Lab Trauma Burns & Combined Injury Chongqing Peoples R China Univ Chinese Acad Sci Chinese Acad Sci Ctr Chongqing Coll Chongqing Peoples R China Kunming Med Univ Dept Cardiol Affiliated Hosp 1 Kunming Yunnan Peoples R China

Aims: Doxorubicin is a powerful chemotherapeutic agent for cancer, whose use is limited due to its potential cardiotoxicity. Semaglutide (SEMA), a novel analog of glucagon-like peptide-1 (GLP-1), has received widespread attention for the treatment of diabetes. However, increasing evidence has highlighted its potential therapeutic benefits on cardiac function. Therefore, the objective of this study was to examine the efficacy of semaglutide in ameliorating doxorubicin-induced cardiotoxicity. Methods and results: Doxorubicin-induced cardiotoxicity is an established model to study cardiac function. Cardiac function was studied by transthoracic echocardiography and invasive hemodynamic monitoring. The results showed that semaglutide significantly ameliorated doxorubicin-induced cardiac dysfunction. RNA sequencing suggested that bnip3 is the candidate gene that impaired the protective effect of semaglutide in doxorubicininduced cardiotoxicity. To determine the role of bnip3 on the effect of semaglutide in doxorubicin-induced cardiotoxicity, bnip3 with adeno-associated virus serotype 9 (AAV9) expressing cardiac troponin T (cTnT) promoter was injected into tail vein of C57/BL6J mice to overexpress bnip3, specifically in the heart. Overexpression of bnip3 prevented the improvement in cardiac function caused by semaglutide. In vitro experiments showed that semaglutide, via PI3K/AKT pathway, reduced bnip3 expression in the mitochondria, improving mitochondrial function. Conclusion: Semaglutide ameliorates doxorubicin-induced mitochondrial and cardiac dysfunction via PI3K/AKT pathway, by reducing bnip3 expression in mitochondria. The improvement in mitochondrial function reduces doxorubicin-mediated cardiac injury and improves cardiac function. Therefore, semaglutide is a potential therapy to reduce doxorubicin-induced acute cardiotoxicity.

关键词： bnip3 Doxorubicin-induced cardiotoxicity Mitochondria PI3K/AKT Semaglutide

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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

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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-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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Down-regulation of bnip3 by olomoucine, a CDK inhibitor, reduces LPS- and NO-induced cell death in BV2 microglial cells

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NEUROSCIENCE LETTERS 2016年第0期628卷 186-193页

作者： Tsou, Yu-Chi Wang, Hsiao-Hsien Hsieh, Chii-Cheng Sun, Kuang-Hui Sun, Guang-Huan Jhou, Ren-Shiang Liu, Tz-I Lu, Shou-Yun Liu, Huan-Yun Tang, Shye-Jye Natl Taiwan Ocean Univ Dept Biosci & Biotechnol Ctr Excellence Oceans Keelung 20224 Taiwan Cheng Hsin Gen Hosp Urol Sect Taipei 11211 Taiwan Natl Yang Ming Univ Dept Biotechnol & Lab Sci Med Taipei 11211 Taiwan Taipei City Hosp Dept Educ & Res Taipei 100 Taiwan Triserv Gen Hosp Div Urol Dept Surg Natl Def Med Ctr Taipei 11100 Taiwan Taoyuan Armed Forces Gen Dept Surg Div Urol Taoyuan Taiwan

Proinflammatory responses eliciting the microglial production of cytokines and nitric oxide (NO) have been reported to play a crucial role in the acute and chronic pathogenic effects of neurodegeneration. Chemical inhibitors of cyclin-dependent kinases (CDKs) may prevent the progression of neurodegeneration by both limiting cell proliferation and reducing cell death. However, the mechanism underlying the protective effect of CDK inhibitors on microglia remains unexplored. In this study, we found that olomoucine, a CDK inhibitor, alleviated lipopolysaccharide (LPS)-induced BV2 microglial cell death by reducing the generation of NO and inhibiting the gene expression of proinflammatory cytokines. In addition, olomoucine reduced inducible NO synthase promoter activity and alleviated NF-kappa B- and E2F-mediated transcriptional activation. NO -induced cell death involved mitochondrial disruptions such as cytochrome c release and loss of mitochondrial membrane potential, and pretreatment with olomoucine prior to NO exposure reduced these disruptions. Microarray analysis revealed that olomoucine treatment induced prominent down-regulation of Bc12/adenovirus El B 19-kDa-interacting protein 3 (bnip3), a pro-apoptotic Bcl-2 family protein that is involved in mitochondrial disruption. As bnip3 knock-down significantly increased the viability of LPS- and NO-treated BV2 cells, we conclude that olomoucine may protect cells by limiting proinflammatory responses, thereby reducing NO generation. Simultaneously, down-regulation of bnip3 prevents NO stimulation from inducing mitochondrial disruption. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

关键词： Microglia BV2 cells Nitric oxide Inflammation bnip3 Olomoucine

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