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Acetyl-coenzyme A acyltransferase 2 attenuates the apoptotic effects of bnip3 in two human cell lines

BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS 2008年第6期1780卷 873-880页

作者： Cao, Wei Liu, Nansong Tang, Shuai Bao, Lei Shen, Li Yuan, Hanying Zhao, Xin Lu, Hong Fudan Univ Sch Life Sci Inst Genet State Key Lab Genet Engn Shanghai 200433 Peoples R China McGill Univ Dept Anim Sci Ste Anne De Bellevue H9X3V9 PQ Canada

bnip3 is a unique pro-apoptotic protein which belongs to the BH3-only subset of the Bcl-2 family and localizes on mitochondrial membrane. Despite the inherent difficulty of identifying binding partners for membrane proteins, several binding partners for bnip3 have been identified. In this study, a modified split-ubiquitin membrane yeast two-hybrid system was constructed and used to identify acetyl-Coenzyme A acyltransferase 2 (ACAA2) as a new bnip3 binding partner. The interaction between bnip3 and ACAA2 was confirmed by pull-down and co-immunoprecipitation assays. ACAA2 was also found to co-localize with bnip3 in mitochondria. Furthermore, the apoptosis induced by over-expressed bnip3 via transfection OF hypoxia treatment was abolished by ACAA2 in human hepatocellular carcinoma HepG2 cells and osteosarcoma U-2 OS cells. These results strongly suggest that ACAA2 be a functional bnip3 binding partner and provide a possible linkage between fatty acid metabolism and apoptosis of cells. (c) 2008 Elsevier B.V. All rights reserved.

关键词： bnip3 ACAA2 split-ubiquitin membrane yeast two-hybrid system apoptosis mitochondrial membrane potential

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Roles of HIF1α- and HIF2α-regulated bnip3 in hypoxia-induced injury of neurons

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PATHOLOGY RESEARCH AND PRACTICE 2019年第4期215卷 822-827页

作者： Zhu, Lei Qi, Boxiang Hou, Daorong Xuzhou Med Univ Xuzhou Childrens Hosp Dept Intens Care Unit Xuzhou 227006 Jiangsu Peoples R China Nanjing Med Univ Key Lab Model Anim Res Anim Core Facil 101 Longmian Ave Nanjing 211166 Jiangsu Peoples R China

Background: To explore the roles of HIF1 alpha- and HIF2 alpha-regulated bnip3 in hypoxia-induced injury of neurons. Methods: The sera of neonates with hypoxic-ischemic encephalopathy (HIE) within 24 h after birth and full-term healthy newborns (n = 40) were collected. The bnip3 levels were detected by ELISA. *** cells were cultured in 1% O-2 at 37 degrees C. The apoptosis of cells treated with 1, 5 and 10 ng/ml bnip3 for 48 h was detected by flow cytometry. The proliferation of cells transfected with sibnip3 was detected by CCK-8 assay. The mRNA level of bnip3 in cells under hypoxic conditions was measured by RT-PCR. The protein level of bnip3 in cells cultured under hypoxic conditions after pretreatment with HIF1 alpha or HIF2 alpha inhibitor was measured by Western blot. Results: The serum bnip3 concentration of HIE neonates ((4.5 +/- 2.1) ng/ml) was significantly higher than that of healthy neonates ((1.2 +/- 0.5) ng/ml) (P < 0.001). Compared with untreated group, the number of apoptotic *** cells treated with bnip3 significantly increased (P < 0.05). Under hypoxic conditions (1%), the mRNA and protein levels of bnip3 increased significantly with prolonged time. After pretreatment with HIF1 alpha or HIF2 alpha inhibitor and hypoxic culture, bnip3 expression was significantly lower than that of cells hypoxically cultured only. Inhibiting the expression of HIF1 alpha or HIF2 alpha or transfecting with sibnip3 before hypoxic treatment significantly reduced the number of apoptotic cells. Under hypoxic conditions, HIF1 alpha or HIF2 alpha bound bnip3 promoter, which did not occur under normal culture conditions. HIF1 alpha or HIF2 alpha was significantly enriched near the hypoxia response element (HRE) site of bnip3 promoter. Conclusions: bnip3 was involved in the apoptosis of cells undergoing HIE. The HRE site of bnip3 promoter bound HIF to promote its transcription.

关键词： Neonate Hypoxic-ischemic encephalopathy bnip3 Apoptosis HIF

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Transcription Factor TFAP2B Exerts Neuroprotective Effects Targeting bnip3-Mediated Mitophagy in Ischemia/Reperfusion Injury

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MOLECULAR NEUROBIOLOGY 2024年第10期61卷 7319-7334页

作者： Peng, Yong Jia, Jiaoying Zhang, Mingming Ma, Wenjia Cui, Yan Yu, Mengqiang Cent South Univ Xiangya Hosp 2 Dept Neurosurg 139 Renmin Middle Rd Changsha 410011 Hunan Peoples R China

Cerebral ischemia-reperfusion injury (CIRI) leads to malignant brain edema, blood-brain barrier destruction, and neuronal apoptosis. N6-methyladenosine (m6A) RNA modification in CIRI was still limited explored. In this study, MeRIP- and RNA-sequencing were performed of middle cerebral artery occlusion and reperfusion (MCAO/R) rats to find novel potential molecular targets. Transcription factor TFAP2B stood out of which its m6A abundance decreased associated with a marked reduction of its mRNA based on cojoint interactive bioinformatics analysis of the MeRIP- and RNA-sequencing data. It was suggested TFAP2B could have a role in CIRI. Functionally, overexpression of TFAP2B in cultured primary neurons could effectively improve the cell survival and pro-survival autophagy in parallel with reduced cell apoptosis during OGD/R in vitro. Through the RNA-sequencing of TFAP2B overexpressed primary neurons and subsequent validation experiments, it was found that mitophagy receptor bnip3 was one of the important targets of TFAP2B in OGD/R neurons through which TFAP2B could bind to its promoter region for transcriptional activation of bnip3, thereby enhancing bnip3-mediated mitophagy to protect against OGD/R injury of neurons. Lastly, TFAP2B was demonstrated to alleviate the MCAO/R damage to a certain extent in vivo. Although it failed to confirm TFAP2B dysregulation was m6A dependent in current research, this is the first research of TFAP2B in CIRI field with important guiding significance.

关键词： Cerebral ischemia-reperfusion injury MeRIP-sequencing RNA-sequencing TFAP2B Primary neurons bnip3 Mitophagy

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Human Milk Fortification Increases bnip3 Expression Associated With Intestinal Cell Death In Vitro

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JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION 2015年第5期61卷 583-590页

作者： Diehl-Jones, William Archibald, Alyssa Gordon, Joseph W. Mughal, Wajihah Hossain, Zakir Friel, James K. Athabasca Univ Fac Hlth Disciplines Athabasca AB Canada Univ Manitoba Dept Biol Sci Winnipeg MB Canada Univ Manitoba Dept Human Anat & Cell Sci Winnipeg MB Canada Univ Manitoba Fac Nursing Winnipeg MB Canada Univ Manitoba Dept Human Nutr Sci Winnipeg MB Canada

Objectives: The aim of the present study was to determine the in vitro effect(s) of a bovine-based human breast milk fortifier (HMF) on human intestinal cells. HMF increases the expression of BCL2/adenovirus E1B 19 kDa protein-interacting protein (bnip3) and cell death;the prostaglandin analogue misoprostol will rescue this effect. Methods: Cultured intestinal cells were exposed to in vitro-digested human breast milk (BM) + HMF. Intracellular oxidation, cell damage/cell death, and bnip3 expression were measured after exposure. Results: In vitro-digested BM+ HMF significantly increased intracellular oxidation, cell damage, and cell death in enterocyte cell cultures compared with either saline or BM controls, an effect that was rescued by the prostaglandin analogue, misoprostol. bnip3 transcript and bnip3 protein levels were significantly increased in vitro after treatment with BM_HMF. We also provide evidence that transfection of enterocytes with bnip3 increases cell death, an effect that is rescued by a nonfunctional bnip3 splice variant. Conclusions: Our data support the hypothesis that HMF increases intestinal bnip3 in vitro, and that the gene product triggers cell death. We suggest that misoprostol is a promising therapy, which may reduce intestinal cell death.

关键词： bnip3 breast milk cell death human milk fortifier intestinal cells

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Bcl-2 family member Mcl-1 expression is reduced under hypoxia by the E3 ligase FBW7 contributing to bnip3 induced cell death in glioma cells

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CANCER BIOLOGY & THERAPY 2016年第6期17卷 604-613页

作者： Chen, Yongqiang Henson, Elizabeth S. Xiao, Wenyan Shome, Epsita Azad, Meghan B. Burton, Teralee R. Queau, Michelle Sathya, Akshay Eisenstat, David D. Gibson, Spencer B. CancerCare Manitoba Res Inst Oncol & Hematol Winnipeg MB Canada Univ Manitoba Dept Biochem & Med Genet Winnipeg MB Canada Univ Alberta Fac Med & Dent Edmonton AB Canada Univ Alberta Dept Pediat Edmonton AB Canada Univ Alberta Dept Med Genet Edmonton AB Canada Univ Alberta Dept Oncol Edmonton AB Canada

Mcl-1 is an anti-apoptotic Bcl-2 family member that is often over-expressed in the malignant brain tumor glioblastoma (GBM). It has been previously shown that epidermal growth factor receptors up-regulate Mcl-1 contributing to a cell survival response. Hypoxia is a poor prognostic marker in glioblastoma despite the fact that hypoxic regions have areas of necrosis. Hypoxic regions of GBM also highly express the pro-cell death Bcl-2 family member bnip3, yet when bnip3 is overexpressed in glioma cells, it induces cell death. The reasons for this discrepancy are unclear. Herein we have found that Mcl-1 expression is reduced under hypoxia due to degradation by the E3 ligase FBW7 leading to increased hypoxia induced cell death. This cell death is reduced by EGFR activation leading to increased Mcl-1 expression under hypoxia. Conversely, bnip3 is over-expressed in hypoxia at times when Mcl-1 expression is decreased. Knocking down bnip3 expression reduces hypoxia cell death and Mcl-1 expression effectively blocks bnip3 induced cell death. Of significance, bnip3 and Mcl-1 are co-localized under hypoxia in glioma cells. These results suggest that Mcl-1 can block the ability of bnip3 to induce cell death under hypoxia in GBM tumors.

关键词： bnip3 EGFR glioma cells hypoxia and Mcl-1

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Prolyl hydroxylase inhibitor FG-4592 alleviates neuroinflammation via HIF-1/bnip3 signaling in microglia

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BIOMEDICINE & PHARMACOTHERAPY 2024年 173卷 116342-116342页

作者： Ruan, Qianqian Geng, Yanan Zhao, Ming Zhang, Heyang Cheng, Xiang Zhao, Tong Yue, Xiangpei Jiang, Xiufang Jiang, Xiaoxia Hou, Xiao-Yu Zhu, Ling-Ling Beijing Inst Basic Med Sci Beijing 100850 Peoples R China China Pharmaceut Univ Sch Life Sci & Technol State Key Lab Nat Med Nanjing 211198 Jiangsu Peoples R China Nantong Univ Co Innovat Ctr Neuroregenerat Nantong 226019 Peoples R China Xuzhou Med Univ Res Ctr Biochem & Mol Biol Xuzhou 221004 Jiangsu Peoples R China 639 Longmian Ave Nanjing 211198 Jiangsu Peoples R China 27 Taiping Rd Beijing 100850 Peoples R China

Background: Neuroinflammation is responsible for neuropsychiatric dysfunction following acute brain injury and neurodegenerative diseases. This study describes how a hypoxia-inducible factor prolyl hydroxylase (HIF-PHD) inhibitor FG-4592 prevents the lipopolysaccharide (LPS)-induced acute neuroinflammation in microglia. Methods: The distribution of FG-4592 in mouse brain tissues was determined by collision-induced dissociation tandem mass spectrometry. Microglial activation in the hippocampus was analyzed by immunofluorescence. Moreover, we determined the activation of HIF-1 and nuclear factor-kappa B (NF-kappa B) signaling pathways, proinflammatory responses using molecular biological techniques. Transcriptome sequencing and bnip3 silencing were conducted to explore signaling pathway and molecular mechanisms underlying FG-4592 anti-inflammatory activity. Results: FG-4592 was transported into the brain tissues and LPS increased its transportation. FG-4592 promoted the expression of HIF-1 alpha and induced the downstream gene transcription in the hippocampus. Administration with FG-4592 significantly inhibited microglial hyperactivation and decreased proinflammatory cytokine levels following LPS treatment in the hippocampus. The LPS-induced inflammatory responses and the NF-kappa B signaling pathway were also downregulated by FG-4592 pretreatment in microglial cells. Mechanistically, Venn diagram analysis of transcriptomic changes of BV2 cells identified that bnip3 was a shared and common differentially expressed gene among different treatment groups. FG-4592 markedly upregulated the protein levels of bnip3 in microglia. Importantly, bnip3 knockdown aggravated the LPS-stimulated inflammatory responses and partially reversed the protection of FG-4592 against microglial inflammatory signaling and microglial activation in the mouse hippocampus. Conclusions: FG-4592 alleviates neuroinflammation through facilitating microglial HIF-1/bnip3 signaling pathway in mice. Target

关键词： FG-4592 Neuroinflammation Microglia Hippocampus Prolyl hydroxylase bnip3 Hypoxia-inducible factor 1 Transcriptome sequencing Neuropsychiatric diseases

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Attenuation of the cytoprotection induced by hypoxic preconditioning upon transfection with bnip3-siRNA in human neuroblastoma SH-SY5Y cells

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INTERNATIONAL JOURNAL OF NEUROSCIENCE 2023年第8期133卷 908-917页

作者： Lu, Na Bai, Ruiying Liu, Bo Cheng, Weijia Wu, Zekun Xinxiang Med Univ Sch Basic Med Sci Henan Key Lab Med Tissue Regenerat Xinxiang 453003 Henan Peoples R China Xinxiang Med Univ Sch Basic Med Sci Dept Physiol & Pathophysiol Xinxiang Henan Peoples R China

Purpose The aim of this study was to investigate the functional role of hypoxic preconditioning (HPC) in human neuroblastoma cells. Methods bnip3 small-interfering RNA (bnip3-siRNA) sequence was synthesized and used to transfect human neuroblastoma SH-SY5Y cell lines. Thereafter, bnip3 expression at mRNA and protein levels and its effects on the cell proliferation were analyzed. The most effective pair of siRNA was selected to knockdown the expression level of bnip3. Moreover, the effects of HPC on oxygen-glucose deprivation/reperfusion (OGD/R)-induced apoptosis and autophagy in SH-SY5Y cells were explored to further reveal the possible mechanisms underlying HPC. Results bnip3-siRNA attenuated the protective effects of HPC by decreasing the cell viability, increasing the enzymatic activity of caspase-3 and 9, increasing the rate of apoptosis, and increasing the protein expression level of activated caspase-3. Additionally, bnip3-siRNA had no significant influence on the expression level of HIF-1 alpha induced by HPC, while it substantially inhibited HPC-induced bnip3/Beclin1 and autophagy. Conclusions HPC promoted autophagy through regulating bnip3 to reduce OGD/R.

关键词： SH-SY5Y bnip3 Beclin1 hypoxic preconditioning oxygen glucose deprivation reperfusion

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miR-96-5p regulates wound healing by targeting bnip3/FAK pathway

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JOURNAL OF CELLULAR BIOCHEMISTRY 2019年第8期120卷 12904-12911页

作者： Wu, Peng Cao, Yongqian Zhao, Ran Wang, Yibing Shandong Univ Shandong Prov Hosp Dept Burns & Plast Surg 324 Jingwu Rd Jinan 250021 Shandong Peoples R China Linyi Peoples Hosp Dept Burns & Plast Surg Linyi Shandong Peoples R China

Cutaneous wound healing is a highly orchestrated basic biological process and one of the key processes in restoring skin integrity. The role of microRNAs (miRNAs) during this process has raised numerous attention and is poorly explored. The aim of this study is to investigate the potential function of BCL2 interacting protein (bnip3) and its target miRNA, miR-96-5p, in cutaneous wound healing. The results demonstrated that bnip3 was significantly increased and miR-96-5p was obviously decreased during wound healing. Overexpression of bnip3 significantly increased, while inhibition of bnip3 decreased cell proliferation and migration of human primary keratinocytes. miR-96-5p was predicted to be a target miRNA for bnip3 and luciferase reporter assay confirmed that miR-96-5p directly targeted the 3 '-untranslated region of bnip3. Moreover, miR-96-5p overexpression significantly decreased, while miR-96-5p inhibition dramatically increased bnip3 protein expression and focal adhesion kinase (FAK) pathway activation. Furthermore, miR-96-5p inhibited cell proliferation and migration of human primary keratinocytes. Overall, our findings suggest that miR-96-5p might be critical in the regulation of wound healing by mediating bnip3 and FAK pathway.

关键词： bnip3 FAK pathway human primary keratinocyte miR-96-5p wound healing

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DUSP1 alleviates cardiac ischemia/reperfusion injury by suppressing the Mff-required mitochondrial fission and bnip3-related mitophagy via the JNK pathways

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REDOX BIOLOGY 2018年 14卷 576-587页

作者： Jin, Qinhua Li, Ruibing Hu, Nan Xin, Ting Zhu, Pingjun Hu, Shunying Ma, Sai Zhu, Hong Ren, Jun Zhou, Hao Chinese Peoples Liberat Army Gen Hosp Med Sch Chinese PLA Beijing 100853 Peoples R China Tianjin First Cent Hosp Dept Cardiol Tianjin 300192 Peoples R China Emory Univ Dept Human Genet Atlanta GA 30322 USA Univ Wyoming Ctr Cardiovasc Res & Alternat Med Laramie WY 82071 USA

Mitochondrial fission and selective mitochondrial autophagy (mitophagy) form an essential axis of mitochondrial quality control that plays a critical role in the development of cardiac ischemia-reperfusion (IR) injury. However, the precise upstream molecular mechanism of fission/mitophagy remains unclear. Dual-specificity protein phosphatasel (DUSP1) regulates cardiac metabolism, but its physiological contribution in the reperfused heart, particularly its influence on mitochondrial homeostasis, is unknown. Here, we demonstrated that cardiac DUSP1 was downregulated following acute cardiac IR injury. In vivo, compared to wild-type mice, DUSP1 transgenic mice (DUSP1(TG) mice) demonstrated a smaller infarcted area and the improved myocardial function. In vitro, the IR-induced DUSP1 deficiency promoted the activation of JNK which upregulated the expression of the mitochondrial fission factor (Mff). A higher expression level of Mff was associated with elevated mitochondrial fission and mitochondrial apoptosis. Additionally, the loss of DUSP1 also amplified the bnip3 phosphorylated activation via JNK, leading to the activation of mitophagy. Increased mitophagy overtly consumed mitochondrial mass resulting into the mitochondrial metabolism disorder. However, the reintroduction of DUSP1 blunted Mff/bnip3 activation and therefore alleviated the fatal mitochondrial fission/mitophagy by inactivating the JNK pathway, providing a survival advantage to myocardial tissue following IR stress. The results of our study suggest that DUSP1 and its downstream JNK pathway are therapeutic targets for conferring protection against IR injury by repressing Mff-mediated mitochondrial fission and bnip3-required mitophagy.

关键词： Cardiac IR injury Mitochondrial fission Mitophagy Mff bnip3 DUSP1 JNK

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Induction of autophagy biomarker bnip3 requires a JAK2/STAT3 and MT1-MMP signaling interplay in Concanavalin-A-activated U87 glioblastoma cells

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CELLULAR SIGNALLING 2014年第5期26卷 917-924页

作者： Pratt, Jonathan Annabi, Borhane Univ Quebec Lab Oncol Mol Dept Chim Ctr Rech BIOMED Montreal PQ H3C 3P8 Canada

Plant lectins have been considered as possible anti-tumor drugs because of their property to induce autophagic cell death. Given that expression of membrane type-1 matrix metalloproteinase (MT1-MMP) has been found to regulate expression of the autophagy biomarker Bc1-2/adenovirus E1B 19 kDa interacting protein 3 (bnip3), we sought to investigate possible signaling interplay mechanisms between MT1-MMP and bnip3 in Concanavalin-A (ConA) lectin-activated U87 glioblastoma cells. ConA induced acidic vacuole organelle formation as well as bnip3 and MT1-MMP gene and protein expressions, whereas only bnip3 expression was dose-dependently inhibited by the JAK2 tyrosine kinase inhibitor AG490 suggesting a requirement for some STAT-mediated signaling. Gene silencing of MT1-MMP and of STAT3 abrogated ConA-induced STAT3 phosphorylation and bnip3 expression. Correlative analysis shows that STAT3 signaling events occur downstream from MT1-MMP induction. Overexpression of a full length MT1-MMP recombinant protein led to increased bnip3 gene and protein expressions. The cytoplasmic domain of MT1-MMP was also found necessary for transducing STAT3 phosphorylation. Among JAK1, JAK2, JAK3, and TYK2, only JAK2 gene silencing abrogated ConA's effects on MT1-MMP and bnip3 gene and protein expressions. Our study elucidates how MT1-MMP signals autophagy, a process which could contribute to the chemoresistance phenotype in brain cancer cells. (C) 2014 Elsevier Inc. All rights reserved.

关键词： Glioblastoma Concanavalin-A Autophagy JAK/STAT MT1-MMP bnip3

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