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HDAC6 preserves bnip3 expression and mitochondrial integrity by deacetylating p53 at lysine 320

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2024年 691卷 149320页

作者： Lee, Se-In Seo, Yuri Oanh, Hoang Thi Vo, Thi Tuyet Hanh Go, Hyeonbin Kim, Myung hun Lee, Joo-Yong Chungnam Natl Univ Grad Sch Analyt Sci & Technol GRAST Daejeon 305764 South Korea Korea Basic Sci Inst Daejeon 305806 South Korea Chungnam Natl Univ GRAST 99 Daehak Ro Daejeon 305764 South Korea

HDAC6 has been reported as a deacetylase of p53 at multiple lysine residues, associated with the canonical functions of p53, such as apoptosis and tumor suppression. We have previously reported that p53 acetylation at the lysine 320 site accumulates due to the genetic ablation of HDAC6 in mice liver. However, the biological processes affected by K320 acetylation of p53 are yet to be elucidated. In this study, we demonstrate that K320 acetylation of p53 is regulated by HDAC6 deacetylase activity. HDAC6 knockout mouse brains exhibit a significant accumulation of K320 acetylated p53 compared to other tissues. The level of K320 acetylation of p53 inversely correlates with the level of bnip3, a direct target of p53 and essential for mitophagy. Notably, overexpressing the deacetylation mimic K320R mutant p53 restored bnip3 expression in HDAC6 knockout MEFs. Furthermore, we observed that neurons are particularly susceptible to the genetic ablation of HDAC6, impacting bnip3 expression, which inversely correlates with the accumulation of abnormal mitochondria characterized by swollen cristae. Our findings suggest that HDAC6 plays a crucial role in maintaining bnip3 expression by deacetylating p53 at the K320 site, which is linked to the structural integrity of mitochondria.

关键词： Acetylation bnip3 HDAC6 Mitochondria p53

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bnip3 as a new tool to promote healthy brain aging

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AGING CELL 2024年第2期23卷 e14042-e14042页

作者： Neikirk, Kit Marshall, Andrea G. Santisteban, Monica M. Hinton Jr, Antentor Vanderbilt Univ Dept Mol Physiol & Biophys 750 Robinson Res Bldg2200 Pierce Ave Nashville TN 37232 USA Vanderbilt Univ Med Ctr Dept Med Nashville TN USA

The article "Neuronal induction of bnip3-mediated mitophagy slows systemic aging in Drosophila" reveals BCL2-interacting protein 3 as a therapeutic target to counteract brain aging and prolong overall organismal health with age. In this spotlight, we consider the roles of bnip3, a mitochondrial outer membrane protein, in the adult nervous system, including its induction of mitophagy and prevention of dysfunctional mitochondria in the aged brain. Implications for other tissue types to reduce the burden of aging are further considered.

关键词： age-related pathology aging bnip3 mitochondria neuronal

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Fangji Huangqi decoction ameliorates membranous nephropathy through the upregulation of bnip3-mediated mitophagy

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JOURNAL OF ETHNOPHARMACOLOGY 2024年 324卷 117734页

作者： Wang, Yuxin Ma, Yuhua Ke, Yanrong Jiang, Xiaocheng Liu, Jian Xiao, Yang Zheng, Hong Wang, Chaojun Chen, Xue Shi, Manman Tradit Chinese Med Hosp Kunshan Dept Nephrol Kunshan 215300 Jiangsu Peoples R China Shanghai Jiao Tong Univ Ruijin Hosp Sch Med Dept Nephrol Shanghai Peoples R China Nanjing Univ Chinese Med Nanjing Jiangsu Peoples R China

Ethnopharmacological relevance: Fangji Huangqi Decoction (FJHQ), a traditional Chinese medicinal formula outlined in Zhang Zhongjing's "Jin Gui Yao Lue" during the Han Dynasty, is often used to treat conditions characterized by symptoms like edema and dysuria, including membranous nephropathy (MN). Despite its proven clinical effectiveness, the exact mechanisms through which FJHQ acts on MN remain elusive. Aim of the study: This study aimed to investigate whether FJHQ enhances bnip3-mediated mitophagy in podocytes by promoting bnip3 expression and whether this improvement leads to the amelioration of MN. Materials and methods: In this study, by establishing passive Heymann nephritis (PHN) rats, an experimental rat model of MN induced by sheep anti -rat Fx1A serum, we evaluated the effects of FJHQ in vivo. In vitro experiments were carried out by treating primary podocytes with experimental rat serum. Furthermore, the potential mechanism by which FJHQ acts through bnip3 was further examined by transfecting primary podocytes with the siRNA of bnip3 or the corresponding control vector. Results: After 4 weeks, significant kidney damage was observed in the rats in the model group, comparatively, FJHQ markedly decreased urine volume, 24-h urinary protein, blood urea nitrogen (BUN), creatinine (Scr), and increased serum total albumin (ALB). Histology showed that FJHQ caused significant improvements in glomerular hyperplasia, and IgG immune complex deposition in MN rats. JC-1 fluorescence labelling and flow cytometry analysis showed that FJHQ could significantly increase mitochondrial membrane potential in vivo. In the mitochondria of MN model rats, FJHQ was able to down-regulate the expression of P62 and up-regulate the expression of bnip3, LC3B, and LC3 II/LC3 I, according to Western blot and immunofluorescence studies. Furthermore, FJHQ has been shown to significantly up-regulate mitochondrial membrane potential, downregulate P62 expression in mitochondria, and up-regula

关键词： Membranous nephropathy Fangji Huangqi decoction Podocyte Mitophagy bnip3

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The evolutionarily conserved hif-1/bnip3 pathway promotes mitophagy and mitochondrial fission in crustacean testes during hypoxia

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AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY, INTEGRATIVE AND COMPARATIVE PHYSIOLOGY 2023年第1期324卷 R128-R142页

作者： Zhao, Qianqian Sun, Xichao Zheng, Cheng Xue, Cheng Jin, Yiting Zhou, Na Sun, Shengming Shanghai Ocean Univ Key Lab Freshwater Aquat Resources Minist Agr & Rural Affairs Shanghai Peoples R China Shanghai Ocean Univ Minist Sci & Technol Int Res Ctr Marine Biosci Shanghai Peoples R China Macau Univ Sci & Technol State Key Lab Qual Res Chinese Med Macau Peoples R China Macau Univ Sci & Technol Sch Pharm Macau Peoples R China

The hypoxia-inducible factor 1 (HIF-1) cascade is an ancient and strongly evolutionarily conserved signaling pathway that is involved in the hypoxic responses of most metazoans. Despite immense advances in the understanding of the HIF-1-mediated regulation of hypoxic responses in mammals, the contribution of the hif-1 cascade in the hypoxic adaptation of nonmodel invertebrates remains unclear. In this study, we used the oriental river prawn Macrobrachium nipponense for investigating the roles of hif-1-regulated mitophagy in crustacean testes under hypoxic conditions. We identified that the Bcl-2/adenovirus E1B 19-kDa interacting protein (bnip3) functions as a regulator of mitophagy in M. nipponense and demonstrated that hif-1a activates bnip3 by binding to the bnip3 promoter. Hif-1a knockdown suppressed the expression of multiple mitophagy-related genes, and prawns with hif-1a knockdown exhibited higher mortality under hypoxic conditions. We observed that the levels of bnip3 were induced under hypoxic conditions and detected that bnip3 knockdown inhibited the mitochondrial translocation of dynamin-related protein 1 (drp1), which is associated with mitochondrial fission. Notably, bnip3 knockdown inhibited hypoxia-induced mitophagy and aggravated the deleterious effects of hypoxia-induced reactive oxygen species (ROS) production and apoptosis. The experimental studies demonstrated that hypoxia induced mitochondrial fission in M. nipponense via drp1. Altogether, the study elucidated the mechanism underlying hif-1/bnip3-mediated mitochondrial fission and mitophagy and demonstrated that this pathway protects crustaceans against ROS production and apoptosis induced by acute hypoxia.

关键词： bnip3 crustaceans hypoxia hypoxia-inducible factor 1a mitophagy

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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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DNA Methylation-Induced bnip3P1 Expression Promotes Pre-Eclampsia Progression via the miR-128-3p/bnip3 Axis

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JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY 2025年第6期39卷 e70307页

作者： Zhang, Qiqi Zheng, Haoyu Zhang, Muling Nanjing Med Univ Affiliated Huaian Peoples Hosp 1 Dept Obstet Huaian Peoples R China

Pre-eclampsia (PE) is a severe, pregnancy-specific disorder characterized by abnormal trophoblast function, leading to impaired placental development and adverse maternal and fetal outcomes. Despite extensive research, the precise molecular mechanisms underlying PE pathogenesis remain incompletely understood. Emerging evidence suggests that long noncoding RNAs (lncRNAs), particularly pseudogenes, play critical roles in regulating trophoblast function, contributing to PE development. This study aims to investigate the role of the lncRNA pseudogene bnip3P1 in the development of PE, focusing on its regulatory interactions with the miR-128-3p/bnip3 axis and the involvement of DNA methylation in bnip3P1 expression. Placental tissues from PE patients (n = 30) and healthy controls (n = 15) were analyzed for bnip3P1 and bnip3 expression using qRT-PCR, western blot, and immunohistochemistry (IHC). In Vitro functional assays utilizing HTR-8/SVneo and JAR trophoblast cell lines were employed to assess the effects of bnip3P1 overexpression and miR-128-3p/bnip3 interaction on cell proliferation, invasion, migration, and apoptosis. The DNA methylation status of the bnip3P1 promoter was analyzed using methylation-specific PCR (MSP) and demethylation treatment with 5-Azacytidine. Additionally, a PE mouse model induced by SFLT-1 recombinant protein was used to evaluate the role of bnip3P1 In Vivo. bnip3P1 and bnip3 were significantly upregulated in PE placental tissues and were positively correlated with clinical indicators such as blood pressure, albumin-to-creatinine ratio (ACR), and serum uric acid levels. In Vitro, bnip3P1 overexpression inhibited trophoblast cell proliferation, invasion, and migration while promoting apoptosis, effects that were reversed by miR-128-3p overexpression. In Vivo, bnip3P1 overexpression exacerbated PE-like symptoms, including hypertension and proteinuria, while knockdown of bnip3 alleviated these symptoms. Mechanistically, bioinformatics analysis an

关键词： bnip3 DNA methylation, mechanism miR-128-3p pre-eclampsia

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Acid ground nano-realgar processed product inhibits breast cancer by inducing mitophagy via the p53/bnip3/NIX pathway

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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 2023年第22期27卷 3478-3490页

作者： Fang, Jiahui Zou, Xue Gong, Ling Xi, Juan Liu, Yi Yang, Xiaoli Zhang, Xiuqiao Gui, Chun Hubei Univ Chinese Med Coll Pharm Wuhan Hubei Peoples R China Hubei Univ Med Taihe Hosp Dept Pharm Shiyan Hubei Peoples R China Hubei Univ Chinese Med Coll Inspection Wuhan Hubei Peoples R China Hubei Univ Chinese Med Coll Pharm 16 Huangjiahu West Rd Wuhan 430065 Hubei Peoples R China

Breast cancer is a highly prevalent malignancy with the first morbidity and the primary reason for female cancer-related deaths worldwide. Acid ground nano-realgar processed product (NRPP) could inhibit breast cancer cell proliferation and induce autophagy in our previous research;however, the underlying mechanisms are still unclear. Therefore, this research aimed to verify whether NRPP induces breast cancer mitophagy and explore the mitophagy-mediated mechanism. Primarily, rhodamine-123 assay and transmission electron microscopy were applied to detect mitochondrial membrane potential (MMP) and ultrastructural changes in the MDA-MB-435S cells, respectively. Mito-Tracker Green/Lyso-Tracker Red staining, western blot, immunofluorescence and RT-PCR were used to explore molecular mechanisms of NRPP-induced mitophagy in vitro. MDA-MB-435S breast cancer xenograft models were established to assess the activity and mechanisms of NRPP in vivo. Our results showed that NRPP decreased MMP and increased autophagosome numbers in MDA-MB-435S cells and activated mitophagy. Furthermore, mitophagy was consolidated because mitochondria and lysosomes colocalized phenomenology were observed, and the expression of LC3II/I and COXIV was upregulated. Additionally, we found the p53/bnip3/NIX pathway was activated. Finally, NRPP inhibited tumour growth and downregulated the levels of TNF-& alpha;, IL-1 & beta;and IL-6. Necrosis, damaged mitochondria and autophagosomes were observed in xenograft tumour cells, and proteins and mRNA levels of LC3, p53, bnip3 and NIX were increased. Overall, NRPP inhibited MDA-MB-435S cell proliferation and tumour growth by inducing mitophagy via the p53/bnip3/NIX pathway. Thus, NRPP is a promising candidate for breast cancer treatment.

关键词： acid ground nano-realgar processed product breast cancer MDA-MB-435S cell mitophagy p53 bnip3 NIX

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The interaction between adhesion protein 33 (TvAP33) and bnip3 mediates the adhesion and pathogenicity of Trichomonas vaginalis to host cells

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PARASITES & VECTORS 2023年第1期16卷 210-210页

作者： Zhang, Zhenchao Deng, Yangyang Sheng, Wanxin Song, Xiaoxiao Li, Yuhua Li, Fakun Pan, Ying Tian, Xiaowei Yang, Zhenke Wang, Shuai Wang, Mingyong Mei, Xuefang Xinxiang Med Univ Sch Basic Med Sci Dept Pathogen Biol Xinxiang 453003 Henan Peoples R China Xinxiang Med Univ Sch Basic Med Sci Xinxiang Key Lab Pathogen Biol Xinxiang 453003 Henan Peoples R China Xinxiang Med Univ Affiliated Hosp 3 Xinxiang 453003 Henan Peoples R China Xinxiang Med Univ Sch Lab Med Xinxiang Key Lab Immunoregulat & Mol Diagnost Xinxiang 453003 Peoples R China Shangqiu Med Coll Sch Med Technol Shangqiu 476100 Peoples R China

Background Trichomonas vaginalis is a widespread and important sexually transmitted pathogen. Adherence to the surface of the host cell is the precondition for the parasitism and pathogenicity of this parasite. Trichomonas vaginalis adhesion protein 33 (TvAP33) plays a key role in the process of adhesion, but how this protein mediates the adhesion and pathogenicity of T. vaginalis to host cells is *** The expression of TvAP33 in trophozoites was knocked down by small interfering RNA. VK2/E6E7 cells and mice infected with T. vaginalis were used to evaluate the pathogenicity of T. vaginalis. We constructed a complementary DNA library of VK2/E6E7 cells and screened the protein molecules interacting with TvAP33 by the yeast two-hybrid system. The interaction between TvAP33 and bnip3 (Bcl-2 interacting protein 3) was analyzed by co-immunoprecipitation and *** Following knockdown of TvAP33 expression, the number of T. vaginalis trophozoites adhering to VK2/E6E7 cells decreased significantly, and the inhibition of VK2/E6E7 cell proliferation and VK2/E6E7 cell apoptosis and death induced by T. vaginalis were reduced. Animal challenge experiments showed that the pathogenicity of trophozoites decreased following passive immunization with TvAP33 antiserum or blocking of the TvAP33 protein. Immunofluorescence analysis revealed that TvAP33 could bind to VK2/E6E7 cells. Eighteen protein molecules interacting with TvAP33 were identified by the yeast two-hybrid system. The interaction between TvAP33 and bnip3 was further confirmed by co-immunoprecipitation and colocalization. When the expression of both TvAP33 and bnip3 in trophozoites was knocked down by small RNA interference, the number of T. vaginalis adhering to VK2/E6E7 cells and the inhibition of VK2/E6E7 cell proliferation were significantly lower compared to trophozoites with only knockdown of TvAP33 or only bnip3. Therefore, the interaction of TvAP33 and bnip3 in the pathogenesis of T. vagin

关键词： T. vaginalis Adhesion protein 33 bnip3 Interaction Mediate Pathogenicity

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bnip3 as a potential biomarker for the identification of prognosis and diagnosis in solid tumours

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MOLECULAR CANCER 2023年第1期22卷 143-143页

作者： Yu, Qin Fu, Wenhao Fu, Yutang Ye, Wenjing Yan, Huiqiong Yu, Zecheng Li, Ruirui Cai, Yili Chen, Yuxin Wang, Lingyun Wei, Xianqiao Chen, Yangkun Zhang, Yuheng Ying, Huazhong Tang, Furong Dai, Fangwei Han, Wei Hangzhou Med Coll Sch Informat Engn Hangzhou Zhejiang Peoples R China Hangzhou Med Coll Sch Med Imaging Hangzhou Zhejiang Peoples R China Hangzhou Med Coll Ctr Lab Anim Hangzhou 310013 Zhejiang Peoples R China Hangzhou Med Coll Zhejiang Prov Key Lab Lab Anim & Safety Res Hangzhou 310013 Zhejiang Peoples R China Hangzhou Med Coll Sch Clin Med Hangzhou Zhejiang Peoples R China Hangzhou Med Coll Sch Med Lab & Biol Engn Hangzhou Zhejiang Peoples R China Hangzhou Med Coll Engn Res Ctr Novel Vaccine Zhejiang Prov Hangzhou Zhejiang Peoples R China Wenzhou Med Univ Quzhou Peoples Hosp Quzhou Affiliated Hosp Quzhou Zhejiang Peoples R China Tsinghua Univ Sch Med Dept Basic Med Sci Beijing Peoples R China

Background Traditional radiotherapy and chemotherapy have been intensively studied for their role in the treatment of tumours. However, these therapies often cause side effects for patients, which calls for the development of novel treatment options for tumours. B-cell lymphoma-2 (Bcl-2)/adenovirus E1B 19 kDa-interacting protein 3 (bnip3) reportedly apoptosis-inducing effects in tumour cells and is associated with the progression and treatment of multiple tumours. Nevertheless, little is known about its potential role in tumour diagnosis and targeted therapy. Findings The results of the study demonstrated that the interaction of bnip3 with HDAC1 may affect the progression of breast invasive cancer (BRCA), sarcoma (SARC), kidney renal clear cell carcinoma (KIRC), and low-grade glioma (LGG). bnip3 seemed to exert its effects in BRCA and SARC primarily through gene silencing and integrator complex, and in KIRC and LGG, mainly by affecting olfactory function, suggesting that targeted therapy can be developed based on the above signalling pathway and downstream molecules. Interpretation bnip3 has emerged as a promising therapeutic and diagnostic target for BRCA, SARC, KIRC, and LGG, providing new insights into tumour molecular therapies in the clinic.

关键词： bnip3 Immune infiltration Pan-cancer analysis Prognostic biomarker Diagnosis

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bnip3 and Nix: Atypical regulators of cell fate

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BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH 2022年第10期1869卷 119325页

作者： Field, Jared T. Gordon, Joseph W. Univ Manitoba Dept Human Anat & Cell Sci Rady Fac Hlth Sci Winnipeg MB Canada Univ Manitoba Coll Nursing Rady Fac Hlth Sci Winnipeg MB Canada Theme Childrens Hosp Res Inst Manitoba Diabet Res Envisioned & Accomplished Manitoba DRE Winnipeg MB Canada

Since their discovery nearly 25 years ago, the BCL-2 family members bnip3 and bnip3L (aka Nix) have been labelled 'atypical'. Originally, this was because bnip3 and Nix have divergent BH3 domains compared to other BCL-2 proteins. In addition, this atypical BH3 domain is dispensable for inducing cell death, which is also unusual for a 'death gene'. Instead, bnip3 and Nix utilize a transmembrane domain, which allows for dimerization and insertion into and through organelle membranes to elicit cell death. Much has been learned regarding the biological function of these two atypical death genes, including their role in metabolic stress, where bnip3 is responsive to hypoxia, while Nix responds variably to hypoxia and is also down-stream of PKC signaling and lipotoxic stress. Interestingly, both bnip3 and Nix respond to signals related to cell atrophy. In addition, our current view of regulated cell death has expanded to include forms of necrosis such as necroptosis, pyroptosis, ferroptosis, and permeability transition-mediated cell death where bnip3 and Nix have been shown to play context- and cell-type specific roles. Perhaps the most intriguing discoveries in recent years are the results demonstrating roles for bnip3 and Nix outside of the purview of death genes, such as regulation of proliferation, differentiation/maturation, mitochondrial dynamics, macro- and selective-autophagy. We provide a historical and unbiased overview of these 'death genes', including new information related to alternative splicing and post-translational modification. In addition, we propose to redefine these two atypical members of the BCL-2 family as versatile regulators of cell fate.

关键词： Nix bnip3 Regulated cell death Proliferation Autophagy Mitophagy

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