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Therapeutic effect of Sirtuin 3 on ameliorating nonalcoholic fatty liver disease: The role of the ERK-CREB pathway and bnip3-mediated mitophagy

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REDOX BIOLOGY 2018年 18卷 229-243页

作者： Li, Ruibing Xin, Ting Li, Dandan Wang, Chengbin Zhu, Hang Zhou, Hao Chinese Peoples Liberat Army Gen Hosp Med Sch Chinese PLA Beijing Peoples R China Tianjin First Cent Hosp Dept Cardiol Tianjin 300192 Peoples R China Wyoming Univ Ctr Cardiovasc Res & Alternat Med Laramie WY 82071 USA

Increased mitochondrial damage is related to the progression of a diet-induced nonalcoholic fatty liver disease. The aim of our study is to investigate the role of Sirtuin 3 (Sirt3) in treating nonalcoholic fatty liver disease with a focus on mitophagy and the ERK-CREB pathway. Our data indicated that Sirt3 was downregulated in liver tissue in response to chronic HFD treatment. Interestingly, re-introduction of Sirt3 protected hepatic function, attenuated liver fibrosis, alleviated the inflammatory response, and prevented hepatocyte apoptosis. Molecular investigations demonstrated that lipotoxicity was associated with an increase in mitochondrial apoptosis as evidenced by reduced mitochondrial potential, augmented ROS production, increased cyt-c leakage into the nucleus, and activated caspase-9 apoptotic signalling. Additionally, Sirt3 overexpression protected hepatocytes against mitochondrial apoptosis via promoting bnip3-required mitophagy. Functional studies showed that Sirt3 reversed bnip3 expression and mitophagy activity via the ERK-CREB signalling pathway. Blockade of the ERK-CREB axis repressed the promotive effects of Sirt3 on bnip3 activation and mitophagy augmentation, finally negating the anti-apoptotic influences of Sirt3 on hepatocytes in the setting of high-fat-stress. Collectively, our data show that high-fat-mediated liver damage is associated with Sirt3 downregulation, which is followed by ERK-CREB pathway inactivation and bnip3-mediated inhibition of mitophagy, causing hepatocytes to undergo mitochondria-dependent cell death. Based on this, strategies for enhancing Sirt3 activity and activating the ERK-CREB-bnip3-mitophagy pathways could be used to treat nonalcoholic fatty liver disease.

关键词： Nonalcoholic fatty liver disease Mitophagy bnip3 Sirt3 ERK-CREB signalling pathway

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The interplay between epigenetic silencing, oncogenic KRas and HIF-1 regulatory pathways in control of bnip3 expression in human colorectal cancer cells

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2013年第4期441卷 707-712页

作者： Swiderek, Ewelina Kalas, Wojciech Wysokinska, Edyta Pawlak, Alicja Rak, Janusz Strzadala, Leon Polish Acad Sci Ludwik Hirszfeld Inst Immunol & Expt Therapy Wroclaw Poland McGill Univ Montreal Childrens Hosp Res Inst Montreal PQ H3A 2T5 Canada

Bcl-2/adenovirus E1B-19 kDa-interacting protein 3 (bnip3) is an important mediator of cell survival and a member of the Bcl-2 family of proteins that regulate programmed cell death and autophagy. We have previously established a link between the expression of oncogenic HRas and up-regulation of bnip3 and the control of autophagy in cancer cells. However, in view of varied expression of bnip3 in different tumor types and emerging uncertainties as to the role of epigenetic silencing, oncogenic regulation and the role of bnip3 in cancer are still poorly understood. In the present study we describe profound effect of KRas on the expression of methylated bnip3 in colorectal cancer cells and explore the interplay between HIF-1, hypoxia pathway and oncogenic KRas in this context. We observed that bnip3 mRNA remains undetectable in aggressive DLD-1 cells harboring G13D mutant KRAS and HT-29 colorectal cancer cells unless the cells are exposed to demethylating agents such as 5-aza-2'-deoxycytidine. Following this treatment bnip3 expression remains uniquely dependent on the Ras activity. We found that hypoxia or pharmacological activation of HIF-1 alone contributes to, but is not sufficient for efficient induction of bnip3 mRNA transcription in cells lacking mutant KRas activity. The up-regulation of bnip3 by KRas in this setting is mediated by the MAPK pathway, and is attenuated by the respective inhibitors (PD98059, U0126). Thus, we demonstrate the novel mechanism where activity of Ras is essential for 5-aza-2'-deoxycytidine-mediated bnip3 expression. Moreover, we found that 5-aza-2'-deoxycytidine-mediated or enforced up-regulation of bnip3 in DLD-1 cells results in KRas-dependent resistance to 5-Fluorouracil. (C) 2013 Elsevier Inc. All rights reserved.

关键词： 5-Aza-2 '-deoxycytidine bnip3 Colorectal cancer HIF-1 Hypoxia KRas

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Expression of bnip3 and its correlations to hypoxia-induced autophagy and clinicopathological features in salivary adenoid cystic carcinoma

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CANCER BIOMARKERS 2015年第4期15卷 467-475页

作者： Chen, Zhanwei Wu, Haiwei Huang, Shengyun Li, Wengang Zhang, Shizhou Zheng, Peihui Zhou, Xiaoqing Liu, Wenlei Zhang, Dongsheng Shandong Univ Shandong Prov Hosp Dept Oral & Maxillofacial Surg Jinan 250021 Shandong Peoples R China

BACKGROUND: The expression of Bcl-2/adenovirus E1B 19 kDa-interacting protein3 (bnip3) has been explored in many human malignancies, but not in adenoid cystic carcinoma (ACC). OBJECTIVE: This study investigated the clinical significance of expression of bnip3 in ACC tissues and cells and elucidated its correlations to hypoxia-induced autophagy. METHODS: Immunohistochemical and immunofluorescence staining were used to explore bnip3, HIF-1 alpha and LC3 expression. RESULTS: bnip3 was positively expressed in 41 cases (63.1%), and was significantly correlated with histological grade (P = 0.001). HIF-1 alpha was positively expressed in 52 cases (80.0%) and was significantly correlated with TNM stage (P = 0.023) and histological grade (P = 0.024). LC3 was positively expressed in 37 cases (56.9%) and was significantly correlated with TNM stage (P = 0.019). The expression of bnip3 was correlated with HIF-1 alpha expression (P = 0.011). The overall survival in the negative bnip3 expression group tended to be better than in the positive bnip3 expression (P = 0.011). In vitro experiment, bnip3 immunofluorescence staining was detected in cells treated with CoCl2 (for hypoxic condition). CONCLUSIONS: The data indicated that bnip3 plays a vital role in the tumorigenesis of adenoid cystic carcinoma and could be a new target for gene therapy of adenoid cystic carcinoma.

关键词： Adenoid cystic carcinoma hypoxia bnip3 HIF-1 alpha autophagy

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Popdc1/Bves Functions in the Preservation of Cardiomyocyte Viability While Affecting Rac1 Activity and bnip3 Expression

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JOURNAL OF CELLULAR BIOCHEMISTRY 2017年第6期118卷 1505-1517页

作者： Kliminski, Vitaly Uziel, Orit Kessler-Icekson, Gania Tel Aviv Univ Sackler Fac Med Felsenstein Med Res Ctr Tel Aviv Israel Tel Aviv Univ Rabin Med Ctr Tel Aviv Israel

The Popeye domain containing1, also called Bves (Popdc1/Bves), is a transmembrane protein that functions in muscle regeneration, heart rate regulation, hypoxia tolerance, and ischemia preconditioning. The expression of Popdc1/Bves is elevated in cardiomyocytes maintained in serum free defined medium. We hypothesized that Popdc1/Bves is important for cardiomyocyte survival under the stress of serum deprivation and investigated the mechanisms involved. A deficit in Popdc1/Bves, achieved by siRNA-mediated gene silencing, results in cardiomyocyte injury and death, upregulation of the pro-apoptotic protein Bcl-2/adenovirus E1B 19-kDa interacting protein3 (bnip3), as well as reduction in Rac1-GTPase activity and in Akt phosphorylation. Combined Popdc1/Bves and bnip3 silencing attenuated cell injury and prevented bnip3 upregulation induced by the silencing of Popdc1/Bves alone. Chromatin immunoprecipitation indicated an increased binding of the transcription factor FoxO3 to the bnip3 promoter although augmentation of FoxO3 in the nuclei was not detected. By contrast, the transcription factor NFB was excluded from the nuclei of Popdc1/Bves deficient cardiomyocytes and exhibited decreased binding to the bnip3 promoter. The data indicates that Popdc1/Bves plays a role in the preservation of cardiomyocyte viability under serum deficiency through the alteration of Rac1 activity and the regulation of bnip3 expression by FoxO3 and NFB transcription factors pointing to Popdc1/Bves as a potential target to enhance heart protection. J. Cell. Biochem. 118: 1505-1517, 2017. (C) 2016 Wiley Periodicals, Inc.

关键词： CARDIOMYOCYTES Popdc1/Bves CELL VIABILITY bnip3 Rac1

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Cobaltosic oxide-polyethylene glycol-triphenylphosphine nanoparticles ameliorate the acute-to-chronic kidney disease transition by inducing bnip3-mediated mitophagy

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KIDNEY INTERNATIONAL 2023年第5期103卷 903-916页

作者： Qin, Shaozong Liu, Chi Chen, Yin Yao, Mengying Liao, Shuyi Xin, Wang Gong, Shuiqin Guan, Xu Li, Yan Xiong, Jiachuan Chen, Jing Shen, Yunzhu Liu, Yong Zhao, Jinghong Huang, Yinghui Army Med Univ Mil Med Univ 3 Xinqiao Hosp Chongqing Clin Res Ctr Kidney & Urol DisDept Neph Chongqing Peoples R China Army Med Univ Mil Med Univ 3 Inst Combined Injury Coll Prevent MedChongqing Engn Res Ctr NanomedSt Chongqing Peoples R China Army Med Univ Mil Med Univ 3 Xinqiao Hosp Chongqing Clin Res Ctr Kidney & Urol DisDept Neph 83 Xinqiao St Chongqing 400037 Peoples R China

Accumulating evidence highlights mitochondrial dysfunction as a crucial factor in the pathogenesis of acute kidney injury (AKI);thus, novel therapeutic strategies maintaining mitochondrial homeostasis are highly anticipated. Recent studies have shown that cobaltosic oxide has peroxidase-like catalytic activities, although its role and mechanism remain elusive in AKI. In the present study, we synthesized and identified cobaltosic oxide -polyethylene glycol-triphenylphosphine (COPT) nanoparticles by conjugating cobaltosic oxide with polyethylene glycol and triphenylphosphine, to improve its biocompatibility and mitochondria-targeting property. We found that COPT preferentially accumulated in the kidney proximal tubule cells, and significantly alleviated ischemic AKI in mouse models and gentamicin induced-AKI in the zebrafish model. COPT also inhibited the transition from AKI to chronic kidney disease (CKD), with few side effects. Further studies demonstrated that COPT localized in the mitochondria, and ameliorated hypoxia-reoxygenation-mediated mitochondrial damage through enhancing mitophagy in vitro and in vivo. Mechanistically, COPT dose -dependently induced the expression of Bcl-2/adenovirus E1B 19-kDa interacting protein (bnip3), while knockdown of bnip3 attenuated COPT-induced mitophagic flux and mitochondrial protection. Thus, our findings suggest that COPT nanoparticles ameliorate AKI and its progression to CKD through inducing bnip3-mediated mitophagy, indicating that COPT may serve as a promising mitochondria-targeting therapeutic agent against AKI.

关键词： acute kidney injury bnip3 chronic kidney disease COPT mitophagy

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Transcriptional regulation of bnip3 by Sp3 in prostate cancer

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PROSTATE 2015年第14期75卷 1556-1567页

作者： Huang, Ying Shen, Pengfei Chen, Xueqin Chen, Zhibin Zhao, Tao Chen, Ni Gong, Jing Nie, Ling Xu, Miao Li, Xinglan Zeng, Hao Zhou, Qiao Sichuan Univ West China Hosp Dept Pathol & Lab Pathol Chengdu 610041 Peoples R China Fujian Prov Hosp Dept Pathol Fuzhou Peoples R China Sichuan Univ West China Hosp Dept Urol Chengdu 610041 Peoples R China

BACKGROUNDThe transcription factors Sp3/Sp1 are expressed in a various types of cancers and bnip3 is overexpressed in prostate cancer. Although it has been demonstrated that bnip3 is transcriptionally regulated by HIF-1 and is post-transcriptionally regulated by miR145, our previous data indicated that there might be some other transcription factors regulating bnip3 in prostate cancer. This study is conducted to investigate whether bnip3 expression is directly regulated by Sp3/Sp1 or not. MATERIALS AND METHODSBioinformatics analysis shows that bnip3 promoter contains several potential Sp3/Sp1 binding sites. And then it is demonstrated that SP3 could regulate the bnip3 transcriptionally by binding to the predicted sites by dual reporter gene assays, ChIP, and EMSA. The biological effects of SP3 regulating bnip3 on prostate cancer cells proliferation are measured by MTT, TUNEL, and flow cytometry. RESULTSOur data show that Sp3 but not Sp1, is positively related to bnip3 overexpression in prostate cancer. Sp3 can directly regulate bnip3 transcription by mainly binding to the Sp3 binding sites (-624 approximate to-615 and -350 approximate to-343) of bnip3 promoter. Knockdown of Sp3 by RNA interference could reduce cells growth and lead to cells apoptosis in PC-3 and DU145. Sp3-dependent bnip3 overexpression might be an important mechanism to promote prostate cancer cells proliferation. CONCLUSIONThis is the first study to provide direct evidence of Sp3-dependent bnip3 expression. Sp3 might be the major transcriptional regulator of bnip3 in prostate cancer and it is worthy to further study. The regulation of bnip3 by Sp3 may be a new cancer-specific therapeutic target in prostate cancer. Prostate 75:1556-1567, 2015. (c) 2015 Wiley Periodicals, Inc.

关键词： prostate cancer Sp3 bnip3 transcriptional regulation proliferation

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RNA methylation reading protein YTHDF2 relieves myocardial ischemia-reperfusion injury by downregulating bnip3 via m⁶A modification

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HUMAN CELL 2023年第6期36卷 1948-1964页

作者： Cai, Xinyong Zou, Pengtao Hong, Lang Chen, Yanmei Zhan, Yuliang Liu, Yuanyuan Shao, Liang Nanchang Med Coll Affiliated Hosp 1 Jiangxi Prov Peoples Hosp Dept Cardiol 92 Aiguo Rd Nanchang 330006 Jiangxi Peoples R China

bnip3 is reported to be involved in hypoxia-induced mitochondrial defect and cell death in cardiomyocytes. However, little is known about the specific function and molecular mechanism of bnip3-mediated mitophagy in myocardial ischemia-reperfusion injury (MIRI). Herein, this study explored the mechanism regulating bnip3-modulated mitophagy in MIRI. Rat cardiomyocytes (H9c2 cells) underwent transfection and hypoxia/reoxygenation (H/R) treatment, followed by cell viability and apoptosis detection. Gain-of-function assays were conducted in rats before MIRI modeling, followed by the monitoring of cardiac changes and the evaluation of cardiac function, myocardial infarction area, and apoptosis in myocardial tissues. The levels of creatine kinase MB (CK-MB), cardiac troponin I (cTnI), lactic dehydrogenase (LDH), reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), p62, and LC3 II/LC3 I were tested in rat serum or H9c2 cells. The co-localization of LC3 and TOMM20 was analyzed. The interaction of bnip3 with YTHDF2 was assessed. H/R treatment decreased cell viability and p62 and SOD levels while elevating cell apoptosis, the levels of CK-MB, cTnI, LDH, MDA, ROS, and LC3 II/LC3 I, the number of autophagosomes, and the co-localization of LC3 and TOMM20 in cardiomyocytes, which were neutralized by downregulating bnip3 or upregulating YTHDF2. Moreover, upregulation of YTHDF2 repressed myocardial injury and mitophagy in MIRI rats. Mechanistically, YTHDF2 mediated bnip3 expression by recognizing methylated bnip3. Upregulation of bnip3 counteracted the suppressive effect of YTHDF2 overexpression on H/R-induced injury and mitophagy in cardiomyocytes. The RNA methylation reading protein YTHDF2 ameliorated MIRI by downregulating bnip3 via m(6)A modification.

关键词： YTHDF2 bnip3 m(6)A modification Mitophagy Myocardial ischemia-reperfusion injury

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Expression of bnip3 correlates with hypoxia-inducible factor (HIF)-1α, HIF-2α and the androgen receptor in prostate cancer and is regulated directly by hypoxia but not androgens in cell lines

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PROSTATE 2008年第3期68卷 336-343页

作者： Shaida, Nadeem Launchbury, Rosalind Boddy, Jane L. Jones, Catherine Campo, Leticia Turley, Helen Kanga, Suresh Banham, Alison H. Malone, Peter R. Harris, Adrian L. Fox, Stephen B. Peter MacCallum Canc Ctr Melbourne Vic 3002 Australia Royal Berkshire Hosp Harold Hopkins Dept Urol Reading Berks England Univ Oxford John Radcliffe Hosp Nuffield Dept Clin Lab Sci Oxford OX1 2JD England Univ Oxford John Radcliffe Hosp Weatherall Inst Mol Med Mol Oncol Lab Oxford OX1 2JD England

BACKGROUND. bnip3 is a hypoxia-induced protein involved in cell death and survival but its role in human tumors is unclear. This study investigated the role of bnip3 in prostate cancer. METHODS. The expression of bnip3, the androgen receptor (AR), hypoxia inducible factor (HIF)-1 alpha, HIF-2 alpha and the hypoxia regulated gene GLUT1 were assessed in tissue microarrays constructed from 149 radical prostatectomy specimens. Statistics compared expression of these factors between each other, conventional clinicopathological parameters and PSA recurrence. Since an association between bnip3 and AR and the HIFs was observed, the influence of hypoxia, clihydrotestosterone and the AR blocker, Casodex, was also investigated in prostate cell lines. RESULTS. bnip3 was expressed in the nucleus and cytoplasm. Eight of 149 (5.5%) tumors showed no expression, 44/149 (29.5%) cases showed exclusively cytoplasmic expression, 17/149 (11.5%) cases showed exclusively nuclear expression and 80/149 (53.5%) cases showed both cytoplasmic and nuclear expression. There was a significant correlation between cytoplasmic bnip3 expression and Gleason score (P = 0.005), age (P = 0.02), AR (P = 0.001), and GLUT1 (P = 0.006). There was a significant correlation between nuclear bnip3 expression and HIF-1 alpha expression (P = 0.006) and HIF-2 alpha expression (P = 0.013) but no correlation between bnip3 and pre-operative PSA, tumor volume, margin positivity or capsular invasion (all P > 0.05). There was an increase in bnip3 expression under conditions of hypoxia (0-1% 02) but not with dihydrotestosterone stimulation or with Casodex treatment. CONCLUSIONS. These findings suggest that bnip3 is directly regulated by hypoxia but that there may be a hormonal independent mechanism coordinating the expression of bnip3 in prostate tumors.

关键词： prostate bnip3 hypoxia autophagy androgen receptor

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Mitophagy defects arising from bnip3 loss promote mammary tumor progression to metastasis

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EMBO REPORTS 2015年第9期16卷 1145-1163页

作者： Chourasia, Aparajita H. Tracy, Kristin Frankenberger, Casey Boland, Michelle L. Sharifi, Marina N. Drake, Lauren E. Sachleben, Joseph R. Asara, John M. Locasale, Jason W. Karczmar, Gregory S. Macleod, Kay F. Univ Chicago Ben May Dept Canc Res Chicago IL 60637 USA Comm Canc Biol Chicago IL USA Comm Mol Metab & Nutr Chicago IL USA Comm Mol Pathogenesis & Mol Med Chicago IL USA Univ Chicago Biomol NMR Facil Chicago IL 60637 USA Beth Israel Deaconess Med Ctr Div Signal Transduct Boston MA 02215 USA Harvard Univ Sch Med Boston MA USA Cornell Univ Div Nutr Sci Ithaca NY USA Univ Chicago Dept Radiol Chicago IL 60637 USA

bnip3 is a hypoxia-inducible protein that targets mitochondria for autophagosomal degradation. We report a novel tumor suppressor role for bnip3 in a clinically relevant mouse model of mammary tumorigenesis. bnip3 delays primary mammary tumor growth and progression by preventing the accumulation of dysfunctional mitochondria and resultant excess ROS production. In the absence of bnip3, mammary tumor cells are unable to reduce mitochondrial mass effectively and elevated mitochondrial ROS increases the expression of Hif-1 alpha and Hif target genes, including those involved in glycolysis and angiogenesistwo processes that are also markedly increased in bnip3-null tumors. Glycolysis inhibition attenuates the growth of bnip3-null tumor cells, revealing an increased dependence on autophagy for survival. We also demonstrate that bnip3 deletion can be used as a prognostic marker of tumor progression to metastasis in human triple-negative breast cancer (TNBC). These studies show that mitochondrial dysfunctioncaused by defects in mitophagycan promote the Warburg effect and tumor progression, and suggest better approaches to stratifying TNBC for treatment.

关键词： bnip3 breast cancer glycolysis HIF-1 alpha invasive carcinoma mitophagy ROS

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Astragalus polysaccharide ameliorates steroid-induced osteonecrosis of femoral head through miR-206/HIF-1α/bnip3 axis

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KAOHSIUNG JOURNAL OF MEDICAL SCIENCES 2021年第12期37卷 1089-1100页

作者： Zhang, Shen-Yao Wang, Fan Zeng, Xiang-Jing Huang, Zhen Dong, Ke-Fang Hunan Univ Chinese Med Dept Orthoped Affiliated Hosp 2 233 CAIERs North Rd Changsha 410005 Peoples R China

Declining autophagy and rising apoptosis are the main factors driving the development of steroid-induced osteonecrosis of the femoral head (SONFH). Here, we showed that astragalus polysaccharide (APS) improved femoral head necrosis via regulation of cell autophagy and apoptosis through microRNA (miR)-206/hypoxia inducible factor-1 (HIF-1 alpha)/BCL2 interacting protein 3 (bnip3) axis. The expression of miR-206, HIF-1 alpha, and bnip3 in SONFH specimens and cell model were measured using qPCR. SONFH cell model was treated with APS. Cell autophagy was evaluated using LC3-immunofluorescence assays. Flow cytometry was conducted to assess cell apoptosis. Apoptosis-related proteins and autophagy-related proteins were determined using western blot. Besides, dual-luciferase reporter assay was employed to investigate the relationship between miR-206 and HIF-1 alpha. Here we showed that miR-206 expression was upregulated in SONFH tissues and cell model. APS promoted autophagy and inhibited apoptosis in SONFH cell model via downregulating miR-206. What is more, HIF-1 alpha was the target of miR-206. Knockdown of HIF-1 alpha reversed the recovery effect of miR-206 inhibitor on SONFH cell model. Furthermore, bnip3 was the target of HIF-1 alpha. HIF-1 alpha overexpression promoted autophagy and inhibited apoptosis, and knockdown of bnip3 abolished the recovery effect of HIF-1 alpha overexpression in SONFH cell model. These results provided evidence that APS reduced miR-206 expression, and the downregulated miR-206 increased bnip3 expression by targeting HIF-1 alpha to promote autophagy and inhibit bone cell apoptosis. Our research proved that APS effectively improved SONFH by regulating cell autophagy and apoptosis.

关键词： astragalus polysaccharide bnip3 HIF-1 alpha miR-206 steroid-induced osteonecrosis of the femoral head

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