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The circular RNA ZNF292 alleviates OGD-induced injury in H9c2 cells via targeting bnip3

Cell Cycle 2019年第23期18卷 3365-3377页

作者： Qi Ren Hu Li Xiaowen Wang Department of Cardiology Jining No.1 People's Hospital Jining China. Affiliated Jining No.1 People's Hospital of Jining Medical University Jining Medical University Jining China.

ABSTRACTABSTRACTThe research aims to explore the roles and regulatory mechanisms of the circular RNA (circRNA) ZNF292 (circZNF292) in OGD-induced damage in H9c2 cells. The H9c2 cells were treated by OGD and/or transfected with circZNF292, si-circZNF292, pc-Bcl-2/adenovirus E1B-19 kDa-interacting protein 3 (bnip3) or corresponding controls. Cell viability was detected with the CCK-8. The protein expression levels of the Bax, caspase-3, Beclin-1, p62, LC3, bnip3, Wnt3a, β-catenin and mammalian target of rapamycin (mTOR) were individually determined via western blot. qRT-PCR was used to examine the circZNF292 expression level. The apoptotic rate was determined by the Annexin V-FITC/PI with flow cytometer. The production of the circZNF292 was promoted by OGD. Abundant circZNF292 released OGD-induced damage by up-regulating cell viability and Wnt3a/β-catenin or mTOR proteins, but down-regulating apoptosis and autophagy. circZNF292 had an opposite effect on these elements mentioned above. Besides, bnip3 was negatively adjusted by the circZNF292. The bnip3 overproduction destroyed the protective effect of circZNF292 on H9c2. circZNF292 released OGD-induced damage in the H9c2 cells by targeting the bnip3 through Wnt/β-catenin and mTOR activation.

关键词： OGD circZNF292 bnip3 ischemic heart disease Wnt/β-catenin mTOR

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Endoplasmic reticulum stress impairs cardiomyocyte contractility through JNK-dependent upregulation of bnip3

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INTERNATIONAL JOURNAL OF CARDIOLOGY 2018年 272卷 194-201页

作者： Bozi, Luiz H. M. Takano, Ana P. C. Campos, Juliane C. Rolim, Natale Dourado, Paulo M. M. Voltarelli, Vanessa A. Wisloff, Ulrik Ferreira, Julio C. B. Barreto-Chaves, Maria L. M. Brum, Patricia C. Univ Sao Paulo Sch Phys Educ & Sport Av Prof Mello Moraes 65 BR-05508900 Butanta SP Brazil Univ Sao Paulo Inst Biomed Sci Dept Anat Sao Paulo Brazil Norwegian Univ Sci & Technol NTNU Dept Circulat & Med Imaging KG Jebsen Ctr Exercise Med Trondheim Norway Univ Sao Paulo Heart Inst BR-05403900 Sao Paulo Brazil Univ Queensland Sch Human Movement & Nutr Sci Brisbane Qld Australia

Background: Disruption of endoplasmic reticulum (ER) homeostasis is a common feature of cardiac diseases. However, the signaling events involved in ER stress-induced cardiac dysfunction are still elusive. Here, we uncovered a mechanism by which disruption of ER homeostasis impairs cardiac contractility. Methods/results: We found that ER stress is associated with activation of JNK and upregulation of bnip3 in a postmyocardial infarction (MI) model of cardiac dysfunction. Of interest, 4-week treatment of MI rats with the chemical ER chaperone 4-phenylbutyrate (4PBA) prevented both activation of JNK and upregulation of bnip3, and improved cardiac contractility. We showed that disruption of ER homeostasis by treating adult rat cardiomyocytes in culture with tunicamycin leads to contractile dysfunction through JNK signaling pathway. Upon ER stress JNK upregulates bnip3 in a FOXO3a-dependent manner. Further supporting a bnip3 mechanism for ER stress-induced deterioration of cardiac function, siRNA-mediated bnip3 knockdown mitigated ER stressinduced cardiomyocyte dysfunction by reestablishing sarcoplasmic reticulum Ca(2+)content. Conclusions: Collectively, our data identify JINK-dependent upregulation of bnip3 as a critical process involved in ER stress-induced cardiomyocyte contractile dysfunction and highlight 4PBA as a potential intervention to counteract ER stress-mediated bnip3 upregulation in failing hearts. (C) 2018 Elsevier B.V. All rights reserved.

关键词： Endoplasmic reticulum Cardiac dysfunction Myocardial infarction INK bnip3 FOX03a

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Yap promotes hepatocellular carcinoma metastasis and mobilization via governing cofilin/F-actin/lamellipodium axis by regulation of JNK/bnip3/SERCA/CaMKII pathways

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REDOX BIOLOGY 2018年 14卷 59-71页

作者： Shi, Chen Cai, Yong Li, Yongheng Li, Ye Hu, Nan Ma, Sai Hu, Shunying Zhu, Pingjun Wang, Weihu Zhou, Hao Peking Univ Canc Hosp & Inst Dept Radiat Oncol Minist Educ Beijing Key Lab Carcinogenesis & Translat Res Beijing Peoples R China Peoples Liberat Army Gen Hosp Canc Ctr Dept Oncol Beijing Peoples R China Univ Wyoming Coll Hlth Sci Ctr Cardiovasc Res & Alternat Med Laramie WY 82071 USA Chinese Peoples Liberat Army Gen Hosp Dept Cardiol Beijing Peoples R China

Despite the increasingly important role of Hippo-Yap in hepatocellular carcinoma (HCC) development and progression, little insight is available at the time regarding the specifics interaction of Yap and cancer cells migration. Here, we identified the mechanism by which tumor-intrinsic Yap deletion resulted in HCC migratory inhibition. Yap was greatly upregulated in HCC and its expression promoted the cells migration. Functional studies found that knockdown of Yap induced JNK phosphorylation which closely bound to the bnip3 promoter and contributed to bnip3 expression. Higher bnip3 employed excessive mitophagy leading to mitochondrial dysfunction and ATP shortage. The insufficient ATP inactivated SERCA and consequently triggered intracellular calcium overload. As the consequence of calcium oscillation, Ca/calmodulin-dependent protein kinases II (CaMKII) was signaled and subsequently inhibited cofilin activity via phosphorylated modification. The phosphorylated cofilin failed to manipulate F-actin polymerization and lamellipodium formation, resulting into the impairment of lamellipodium-based migration. Collectively, our results identified Hippo-Yap as the tumor promoter in hepatocellular carcinoma that mediated via activation of cofilin/F-actin/lamellipodium axis by limiting JNK-bnip3-SERCA-CaMKII pathways, with potential application to HCC therapy involving cancer metastasis.

关键词： Yap JNK bnip3 SERCA CaMKII F-actin Cofilin Lamellipodium Migration

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Akebia saponin D alleviates hepatic steatosis through bnip3 induced mitophagy

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JOURNAL OF PHARMACOLOGICAL SCIENCES 2018年第4期136卷 189-195页

作者： Gong, Li-li Yang, Song Zhang, Wen Han, Fei-fei Lv, Ya-li Wan, Zi-Rui Liu, He Jia, Yang-jie Xuan, Ling-ling Liu, Li-hong Capital Med Univ Beijing Chao Yang Hosp 8 Gongren Tiyuchang Nanlu Beijing 100020 Peoples R China

Akebia Saponin D (ASD) is the most abundant constituent of the rhizome of Dipsacus asper Wall. The prior studies have shown that ASD alleviates hepatic steatosis targeted at the modulation of autophagy and exerts hepatoprotective effects through mitochondria. However, it is still unclear which signal transduction pathway that ASD increase autophagy and protect the mitochondria. The purpose of this paper was to explore the mechanisms through which ASD alleviates hepatic steatosis. ASD significantly reduced lipid accumulation in BRL cells. Furthermore, ASD significantly increased the mitophagy acting as increase the colocalization between mitochondria and punctate EGFP-LC3. ASD treatment increased the expression of bnip3, phospho-AMPK, prevented oleic acid (OA) induced LC3-II and phospho-mTOR expression. These effects were similar to the effects cotreatment with rapamycin. ASD treatment could not attenuate the expression of bnip3 blocked by chloroquine (CQ) or siRNA-mediated knockdown of bnip3. These results suggest that Akebia saponin D alleviates hepatic steatosis targeted at bnip3 mediated mitophagy. Activation of bnip3 via ASD may offer a new strategy for treating NAFLD. (C) 2018 The Authors. Production and hosting by Elsevier B.V.

关键词： bnip3 Mitophagy NAFLD Akebia saponin D

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Mst1 regulates colorectal cancer stress response via inhibiting bnip3-related mitophagy by activation of JNK/p53 pathway

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CELL BIOLOGY AND TOXICOLOGY 2018年第4期34卷 263-277页

作者： Li, Qi Qi, Feng Meng, Xiangchao Zhu, Chenpei Gao, Yingtang Tianjin Med Univ Dept Gen Surg Cent Clin Coll 3 Tianjin 300170 Peoples R China Tianjin Med Univ Gen Hosp Dept Gen Surg Tianjin 300052 Peoples R China Tianjin Third Cent Hosp Tianjin Key Lab Artificial Cell 83 Jintang Rd Tianjin 300170 Peoples R China

The Hippo-Mst1 pathway is associated with tumor development and progression. However, little evidence is available for its role in colorectal cancer (CRC) stress response via mitochondrial homeostasis. In this study, we conducted gain-of function assay about Mst1 in CRC via adenovirus transfection. Then, cellular viability and apoptosis were measured via MTT, TUNEL assay, and typan blue staining. Mitochondrial function was detected via JC1 staining, mPTP opening assay, and immunofluorescence of cyt-c. Mitophagy was observed via western blots and immunofluorescence. Cell migration and proliferation were evaluated via Transwell and BrdU assay. Western blots were used to analyze the signaling pathways with JNK inhibitors or p53 siRNA. We found that Mst1 was down-regulated in CRC. Overexpression of Mst1 induced CRC apoptosis and impaired cell proliferation and migration. Functional studies have illustrated that recovery of Mst1 could activate JNK pathway which upregulated the p53 expression. The latter repressed bnip3 transcription and activity, leading to the mitophagy arrest. The defective mitophagy impaired mitochondrial homeostasis, evoked cellular oxidative stress, and initiated the mitochondrial apoptosis. Meanwhile, bad-structured mitophagy also hindered the cancer proliferation via CyclinD/E. Moreover, Mst1-suppressed mitophagy was associated with CRC migration inhibition via regulation of CXCR4/7 expression. Collectively, our data described the comprehensive role of Mst1 in colorectal cancer stress response involving apoptosis, mobilization, and growth via handling mitophagy by JNK/p53/bnip3 pathways.

关键词： Mst1 Colorectal cancer Mitophagy p53 bnip3

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Mitophagy mediated by bnip3 and bnip3L/NIX in urothelial cells of the urinary bladder of cattle harbouring bovine papillomavirus infection

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VETERINARY MICROBIOLOGY 2019年 236卷 108396-000页

作者： Roperto, Sante De Falco, Francesca Perillo, Antonella Catoi, Cornel Roperto, Franco Univ Napoli Federico II Dipartimento Med Vet & Prod Anim Naples Italy Univ Bari Aldo Moro Dipartimento Med Vet Valenzano Italy Univ Agr Sci & Vet Med Fac Vet Med Pathol Dept Cluj Napoca Romania Univ Napoli Federico II Dipartimento Biol Naples Italy

Autophagy is a powerful tool that host cells use to defend against viral infection. Mitophagy, the selective autophagic removal of dysfunctional mitochondria was upregulated in urothelial cancer cells harbouring bovine papillomavirus (BPV) infection, as detected by the expression of BPV E5 protein, the major oncoprotein of bovine Deltapapillomavirus genus. HIF-1 alpha-induced mitophagy receptors, bnip3 and bnip3L/Nix, were found to be overexpressed in these cells. The bnip3 and bnip3L/Nix receptors were amplified, and amplicon sequencing showed homology between bovine BNPI3 and bnip3L/Nix sequences deposited in GenBank (accession number: NM_001076366.1 and NM_001034614.2, respectively). The transcripts and protein levels of bnip3 and bnip3L/Nix were significantly overexpressed in hypoxic neoplastic cells relative to healthy, non-neoplastic cells. bnip3 and bnip3L/Nix interacted with the LC3 protein, a marker of autophagosome (mitophagosome) membrane, ERAS, a small GTPase, and p62, known to be a specific autophagy receptor protein, that plays a role in mitochondrial priming for mitophagy and subsequent elimination. ERAS also interacted with the BPV E5 oncoprotein at mitochondrial level. Furthermore, in anti-Bag3 mitochondrial immunoprecipitates, a complex composed of the Hsc70/Hsp70 chaperone, CHIP co-chaperone, Synpo2, ERAS, LC3, p62, BNPI3, and bnip3L/Nix was also detected. Bag3 may play a role in mitophagosome formation together with the Synpo2 protein and may be involved in the degradation of Hsc70/Hsp70-bound CHIP-ubiquitinated cargo, in association with its chaperone. ERAS may be involved in mitophagosome maturation via the PI3K signalling pathway. Ultrastructural findings revealed the presence of mitochondria exhibiting severe fragmentation and loss of cristae, as well as numerous mitochondria-containing autophagosomes.

关键词： BPV E5 oncoprotein bnip3 bnip3L/Nix Mitophagy receptors Bag3 HIF-1 alpha

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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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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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凋亡相关基因BNIP3和DAPK1甲基化与胃癌发生发展、化疗疗效及预后...

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作者：娄萧旗安徽医科大学

学位级别：硕士

背景外周血白细胞bnip3和DAPK1基因甲基化作为胃癌（gastric cancer,GC）检测的无创生物标志物的潜在价值仍有待评估。本研究的目的是检测研究对象外周血白细胞中bnip3和DAPK1基因甲基化水平,并探讨bnip3和DAPK1基因甲基化水平与胃癌发... 详细信息

背景外周血白细胞bnip3和DAPK1基因甲基化作为胃癌（gastric cancer,GC）检测的无创生物标志物的潜在价值仍有待评估。本研究的目的是检测研究对象外周血白细胞中bnip3和DAPK1基因甲基化水平,并探讨bnip3和DAPK1基因甲基化水平与胃癌发生发展、化疗疗效及预后的关联。方法本项研究采用病例对照的研究方法,利用Methyl Target技术检测150例胃癌患者和100例健康对照（healthy controls,HCs）外周血白细胞中bnip3和DAPK1基因甲基化水平。从bnip3基因中挑选出55个Cp G位点,4个区域进行甲基化水平检测;从DAPK1基因挑选出85个Cp G位点,6个区域进行甲基化水平检测。评估bnip3和DAPK1基因甲基化水平与胃癌发生发展、化疗疗效及预后的关联。结果研究结果表明,胃癌患者bnip3和DAPK1基因的38个Cp G位点和6个Cp G岛的甲基化水平低于健康对照(Padj<0.05)。女性中Cp G位点bnip3＿1＿5和bnip3＿s＿1联合检测,诊断特异性和敏感性分别为75.0%,88.9%;DAPK1＿4＿9和DAPK1＿5＿2联合检测,诊断特异性和敏感性分别为66.7%,77.8%。临床病理特征分层分析结果表明:bnip3和DAPK1基因在男性、年轻（≤平均值）、低分化和Ⅳ期胃癌患者中呈现低甲基化;bnip3和DAPK1基因甲基化水平与淋巴结转移、内脏转移和肿瘤部位无关。化疗疗效及预后分析结果表明:胃癌患者bnip3和DAPK1基因甲基化水平与化疗疗效及预后有关,低甲基化患者的化疗疗效比高甲基化患者差,低甲基化患者的DFS,PFS和OS比高甲基化患者明显缩短。结论外周血白细胞bnip3和DAPK1基因甲基化水平与胃癌发生发展及化疗疗效有关,外周血白细胞bnip3和DAPK1基因甲基化水平具有检测胃癌、识别更具侵袭性生物学行为患者和评价患者化疗疗效和预后的潜在价值。

关键词：胃癌 bnip3 DAPK1 甲基化

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RETRACTED: Long non-coding RNA HULC promotes UVB-induced injury by up-regulation of bnip3 in keratinocytes (Retracted article. See vol. 148, 2022)

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BIOMEDICINE & PHARMACOTHERAPY 2018年 104卷 672-678页

作者： Zhao, Li Man, Yigang Liu, Shumei Jining 1 Peoples Hosp Dept Dermatol 6 Jiankang Rd Jining 272011 Peoples R China Jining 1 Peoples Hosp Dept Pediat Jining 272011 Peoples R China

Ultraviolet radiation b (UVB) is a common high-energy radiation which can lead to cell damage and even skin cancer. The mechanisms of lncRNAs in various diseases have attracted much attention of researchers. Herein, we investigated the effects and regulations of lncRNA highly up-regulated in liver cancer (HULC) on UVB-induced injury in HaCaT cells. The HaCaT cells were exposed to UVB at a wavelength of 280-320 nm. Cell viability was detected at different times (0, 3, 6, 12 and 24 h) after UVB treatment. Cells were transfected with sh-HULC, pcHULC, sh-bnip3 (Bcl-2 interacting protein 3) or pc-bnip3, respectively. ZM 39,923 HCl was used as JAK/STAT(1/3) inhibitor. Cell viability and apoptosis were tested by trypan blue dye and flow cytometry analysis, respectively. The expression levels of autophagy-related factors were analyzed by Western blot assay. The expression changes of HULC and bnip3 were measured by qRT-PCR. We found that UVB decreased cell viability, increased apoptosis and autophagy, and up-regulated the expression of HULC in HaCaT cells. Overexpression of HULC reduced cell viability, enhanced apoptosis and autophagy, and up-regulated bnip3 expression by activating JAK/STAT(1/3) signaling pathway. Finally, bnip3 suppression increased cell viability, reduced apoptosis and autophagy via the deactivation of mTOR signaling pathway. The results demonstrated that lncRNA HULC up-regulated bnip3 and activated JAK/STAT(1/3) signaling pathway to accelerate UVB-induced cell damage in HaCaT cells. This study provides a possible target for the clinical treatment of UVB-induced keratinocyte injury.

关键词： lncRNA HULC bnip3 UVB-induced JAK/STAT(1/3) pathway mTOR pathway

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