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Effect of oxygen and glucose availability during in vitro maturation of bovine oocytes on development and gene expression

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JOURNAL OF ASSISTED REPRODUCTION AND GENETICS 2021年第6期38卷 1349-1362页

作者： Whitty, Annie Kind, Karen L. Dunning, Kylie R. Thompson, Jeremy G. Univ Adelaide Adelaide Med Sch Robinson Res Inst Adelaide SA Australia Univ Adelaide Sch Anim & Vet Sci Adelaide SA Australia Univ Adelaide Australian Res Council Inst Photon & Adv Sensing Ctr Excellence Nanoscale BioPhoton Adelaide SA Australia Univ Adelaide Adelaide Med Sch Level 2Helen Mayo South BldgFrome Rd Adelaide SA 5005 Australia

Purpose Oxygen tension during the in vitro maturation (IVM) of oocytes is important for oocyte developmental competence. A conflict exists in the literature as to whether low oxygen during IVM is detrimental or beneficial to the oocyte. Many research and clinical labs use higher than physiological oxygen tension perhaps believing that low-oxygen tension is detrimental to oocyte development. Other studies show that glucose is important if low-oxygen tension is used during maturation. In this study, we look at the link between low oxygen and glucose availability during IVM to resolve misconceptions around low-oxygen tension during IVM. Methods Bovine cumulus oocyte complexes (COCs) were matured at 20% vs 7% oxygen in media containing differing glucose concentrations or varying availability. Cleavage and blastocyst rates were recorded. RT-PCR determined expression levels of metabolic, oxygen, and stress-responsive genes following IVM. Results Embryo development in 7% oxygen groups with 2.3mM glucose/low glucose availability was lower than 20% oxygen groups. Under 7% oxygen with 5.6mM glucose or higher glucose availability, rates were restored to those seen in 20% oxygen. Expressions of bnip3, ENO1, GAPDH, and SLC2A1, were upregulated in 7% oxygen/low glucose, compared to 20% oxygen groups. bnip3 expression was higher in 7% oxygen group with low glucose availability compared to the 20% groups. Conclusion Oocyte developmental competence is negatively impacted following IVM in low oxygen when glucose availability is limited. Glucose concentration and physical culture conditions need to be considered when comparing the effects of different oxygen concentrations during IVM.

关键词： Oocyte Cumulus oocyte complex In vitro maturation Bovine Oxygen Glucose bnip3 ENO1 GAPDH

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Trichomonas vaginalis adhesion protein 65 (TvAP65) modulates parasite pathogenicity by interacting with host cell proteins

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ACTA TROPICA 2023年第1期246卷 106996页

作者： Zhang, Zhenchao Song, Xiaoxiao Deng, Yangyang Li, Yuhua Li, Fakun Sheng, Wanxin Tian, Xiaowei Yang, Zhenke Mei, Xuefang Wang, Shuai 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 Basic Med Sci Xinxiang 453003 Henan Peoples R China

Trichomonas vaginalis (T. vaginalis) is a widespread and important sexually transmitted pathogen. Adherence to the surface of the host cell is the precondition forthis parasite's parasitism and pathogenicity. Adhesion protein 65 (TvAP65) plays a key role in the process of adhesion. However, how TvAP65 mediates the adhesion and pathogenicity of T. vaginalis to host cellsis unclear. In this study, we knocked down the expression of TvAP65 in trophozoites by small RNA interference. The number of T. vaginalis trophozoites adhering to VK2/E6E7 cells was decreased significantly, and the inhibition of VK2/E6E7 cells proliferation and VK2/E6E7 cells apoptosis and death induced by T. vaginalis were reduced, after the expression of TvAP65 was knocked down. Animal challenge experiments showed that the pathogenicity of trophozoites was decreased by passive immunization with antirTvAP65 PcAbs or blocking the TvAP65 protein. Immunofluorescence analysis showed that TvAP65 could bind to VK2/E6E7 cells. In order to screen the molecules interacting with TvAP65 on the host cells, we successfully constructed the cDNA library of VK2/E6E7 cells, and thirteen protein molecules interacting with TvAP65 were screened by yeast two-hybrid system. The interaction between TvAP65 and bnip3 was further confirmed by coimmunoprecipitation and colocalization. When both TvAP65 and bnip3 were knocked down by small RNA interference, the number of T. vaginalis adhering to VK2/E6E7 cells and the inhibition of VK2/E6E7 cells proliferation were significantly lower than those of the group with knockdown of TvAP65 or bnip3 alone. Therefore, the interaction of TvAP65 and bnip3 in the pathogenesis of T. vaginalis infecting host cells is not unique and involves other molecules. Our study elucidated that the interaction between TvAP65 and bnip3 mediated the adhesion and pathogenicity of T. vaginalis to host cells, provided a basis for searching for the drug targets of anti-T. vaginalis, and afforded new ideas for

关键词： T vaginalis adhesion protein 65 bnip3 interaction mediation pathogenicity

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bnip3 Regulates at101 [(-)-Gossypol] Induced Death in Malignant Peripheral Nerve Sheath Tumor Cells

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2016年

作者： niroop kaza

bnip3 Regulates at101 [(-)-Gossypol] Induced Death in Malignant Peripheral Nerve Sheath Tumor Cells. by Kaza, Niroop; Kohli, Latika; Graham, Christopher D.; Klocke, Barbara J.; Carroll, Steven L.; Roth, Kevin A.; publ... 详细信息

关键词： [(-)-gossypol] at101 bnip3 cells. death

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Aryl hydrocarbon receptor maintains hepatic mitochondrial homeostasis in mice

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MOLECULAR METABOLISM 2023年 72卷 101717-101717页

作者： Heo, Mi Jeong Suh, Ji Ho Lee, Sung Ho Poulsen, Kyle L. An, Yu A. Moorthy, Bhagavatula Hartig, Sean M. Moore, David D. Kim, Kang Ho Univ Texas Hlth Sci Ctr Houston Crit Care & Pain Med & Ctr Perioperat Med McGovern Med Sch Dept Anesthesiol Houston TX 77030 USA Chonnam Natl Univ Res Inst Pharmaceut Sci Coll Pharm Gwangju 61186 South Korea Baylor Coll Med Dept Pediat Sect Neonatol Houston TX 77030 USA Texas Childrens Hosp Houston TX 77030 USA Baylor Coll Med Dept Med Div Diabet Endocrinol & Metab Houston TX 77030 USA Baylor Coll Med Dept Mol & Cellular Biol Houston TX 77030 USA Univ Calif Berkeley Dept Nutr Sci & Toxicol Berkeley CA 94720 USA Univ Texas Hlth Sci Ctr Houston McGovern Med Sch Dept Anesthesiol Crit Care & Pain Med 6431 Fannin St Houston TX 77030 USA Univ Calif Berkeley Dept Nutr Sci & Toxicol 119 Morgan Hall Berkeley CA 94720 USA

Objective: Mitophagy removes damaged mitochondria to maintain cellular homeostasis. Aryl hydrocarbon receptor (AhR) expression in the liver plays a crucial role in supporting normal liver functions, but its impact on mitochondrial function is unclear. Here, we identified a new role of AhR in the regulation of mitophagy to control hepatic energy ***: In this study, we utilized primary hepatocytes from AhR knockout (KO) mice and AhR knockdown AML12 hepatocytes. An endogenous AhR ligand, kynurenine (Kyn), was used to activate AhR in AML12 hepatocytes. Mitochondrial function and mitophagy process were compre-hensively assessed by MitoSOX and mt-Keima fluorescence imaging, Seahorse XF-based oxygen consumption rate measurement, and Mitoplate S-1 mitochondrial substrate utilization ***: Transcriptomic analysis indicated that mitochondria-related gene sets were dysregulated in AhR KO liver. In both primary mouse hepatocytes and AML12 hepatocyte cell lines, AhR inhibition strongly suppressed mitochondrial respiration rate and substrate utilization. AhR inhibition also blunted the fasting response of several essential autophagy genes and the mitophagy process. We further identified BCL2 interacting protein 3 (bnip3), a mitophagy receptor that senses nutrient stress, as an AhR target gene. AhR is directly recruited to the bnip3 genomic locus, and bnip3 transcription was enhanced by AhR endogenous ligand treatment in wild-type liver and abolished entirely in AhR KO liver. Mechanistically, overexpression of bnip3 in AhR knockdown cells mitigated the production of mitochondrial reactive oxygen species (ROS) and restored functional ***: AhR regulation of the mitophagy receptor bnip3 coordinates hepatic mitochondrial function. Loss of AhR induces mitochondrial ROS production and impairs mitochondrial respiration. These findings provide new insight into how endogenous AhR governs hepatic mito-chondrial homeostasis.o 2023 The Authors. Pu

关键词： Mitophagy Autophagy Reactive oxygen species bnip3 Kynurenine

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XBP1-mediated activation of the STING signalling pathway in macrophages contributes to liver fibrosis progression

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JHEP REPORTS 2022年第11期4卷 100555-100555页

作者： Wang, Qi Bu, Qingfa Liu, Mu Zhang, Rui Gu, Jian Li, Lei Zhou, Jinren Liang, Yuan Su, Wantong Liu, Zheng Wang, Mingming Lian, Zhexiong Lu, Ling Zhou, Haoming Nanjing Med Univ Chinese Acad Med Sci Affiliated Hosp 1 Key Lab Liver TransplantatNHC Key Lab Liver Tran Nanjing Peoples R China Southeast Univ Sch Med Nanjing Peoples R China Guangdong Acad Med Sci Guangdong Prov Peoples Hosp Guangzhou Peoples R China Nanjing Med Univ Collaborat Innovat Ctr Canc Personalized Med Jiangsu Key Lab Canc Biomarkers Prevent & Treatmen Nanjing Peoples R China Nanjing Med Univ Affiliated Hosp 1 Hepatobiliary Ctr 300 Guang Zhou Rd Nanjing 210029 Peoples R China Guangdong Acad Med Sci Guangdong Prov Peoples Hosp Guangzhou 510080 Peoples R China

Background & Aims: XBP1 modulates the macrophage proinflammatory response, but its function in macrophage stimulator of interferon genes (STING) activation and liver fibrosis is unknown. X-box binding protein 1 (XBP1) has been shown to promote macrophage nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) activation in steatohepatitis. Herein, we aimed to explore the underlying mechanism of XBP1 in the regulation of STING signalling and the subsequent NLRP3 activation during liver ***: XBP1 expression was measured in the human fibrotic liver tissue samples. Liver fibrosis was induced in myeloid -specific Xbp1-, STING-, and Nlrp3-deficient mice by carbon tetrachloride injection, bile duct ligation, or a methionine/choline-deficient ***: Although increased XBP1 expression was observed in the fibrotic liver macrophages of mice and clinical patients, myeloid-specific Xbp1 deficiency or pharmacological inhibition of XBP1 protected the liver against fibrosis. Furthermore, it inhibited macrophage NLPR3 activation in a STING/IRF3-dependent manner. Oxidative mitochondrial injury facilitated cytosolic leakage of macrophage self-mtDNA and cGAS/STING/NLRP3 signalling activation to promote liver fibrosis. Mecha-nistically, RNA sequencing analysis indicated a decreased mtDNA expression and an increased BCL2/adenovirus E1B inter-acting protein 3 (bnip3)-mediated mitophagy activation in Xbp1-deficient macrophages. Chromatin immunoprecipitation (ChIP) assays further suggested that spliced XBP1 bound directly to the bnip3 promoter and inhibited the transcription of bnip3 in macrophages. Xbp1 deficiency decreased the mtDNA cytosolic release and STING/NLRP3 activation by promoting bnip3-mediated mitophagy activation in macrophages, which was abrogated by bnip3 knockdown. Moreover, macrophage XBP1/STING signalling contributed to the activation of hepatic stellate ***: Our findings demonstrate that XBP1

关键词： XBP1 Macrophage Liver fibrosis mtDNA STING bnip3 Mitophagy

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Cordycepin enhances anti-tumor immunity in colon cancer by inhibiting phagocytosis immune checkpoint CD47 expression

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INTERNATIONAL IMMUNOPHARMACOLOGY 2022年第0期107卷 1页

作者： Deng, Qifeng Li, Xinrui Fang, Chunqiang Li, Xin Zhang, Jing Xi, Qing Li, Yan Zhang, Rongxin Guangdong Pharmaceut Univ Guangdong Prov Key Lab Biotechnol Drug Candidates Inst Basic Med Sci Guangzhou Peoples R China Guangdong Pharmaceut Univ Dept Biotechnol Sch Life Sci & Biophammceut Guangzhou Peoples R China Guangdong Pharmaceut Univ Affiliated Hosp 1 Guangzhou Peoples R China South China Univ Technol Sch Biomed Sci & Engn Guangzhou Peoples R China

Cordycepin, also known as 3 '-deoxyadenosine, is an extract from Cordyceps militaris, which has been reported as an anti-inflammation and anti-tumor substance without toxicity. However, the pharmacological mechanism of Cordycepin on tumor immunity under its anti-tumor effect has not yet been elucidated. Herein, we investigated Cordycepin's anti-tumor effect on colon cancer both in vitro and in vivo. Our results show that Cordycepin can inhibit growth, migration, and promoted apoptosis of CT26 cells in a dose-dependent manner. Cordycepin suppressed the growth of colon cancer in mouse subcutaneous tumor model by modulating tumor immune microenvironment where CD4+ T, CD8+ T, M1 type macrophages, NK cells were up-regulated. Further investigations revealed that Cordycepin inhibited phagocytosis immune checkpoint CD47 protein expression by reducing bnip3 expression. In addition, Cordycepin also inhibited the expression of TSP1 in tumor cells and Jurkat cells, which may reduce the binding of TSP1 to CD47, thereby reducing T cell apoptosis and allowing more T cells to infiltrate into tumors. And in vitro co-culture experiments proved that Cordycepin could enhance the phagocytosis of CT26 cells by macrophages. These results explained the underlying mechanism of the antitumor immunity of Cordycepin. In conclusion, our results identify a novel mechanism by which Cordycepin inhibits phagocytosis immune checkpoint CD47 in tumor cells to promote tumor cells phagocytosis of macrophages. Cordycepin may be able to serve as a more effective immunotherapeutic drug against colon cancer.

关键词： Cordycepin Colon Cancer CD47 bnip3 Immune Checkpoint Immune Microenvironment

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中医药调控线粒体自噬防治代谢相关脂肪性肝病机制的研究进展

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天津中医药 2024年第10期41卷 1354-1360页

作者：施雨峰卢晨霞吕安淇肖明中李晓东湖北中医药大学中医临床学院武汉430065 湖北中医药大学附属医院武汉430061 湖北省中医院肝病科中医肝肾研究及应用湖北省重点实验室武汉430061 湖北省中医药研究院武汉430074

代谢相关脂肪性肝病(MAFLD)是一种最常见的代谢性疾病,已成为目前中国最普遍的肝脏疾病,随着病程的进展会对身体和健康产生诸多负面影响,如肝功能受损,MAFLD可导致肝炎、肝纤维化,甚至发展为肝硬化及肝癌;MAFLD还可导致身体代谢紊乱,从... 详细信息

代谢相关脂肪性肝病(MAFLD)是一种最常见的代谢性疾病,已成为目前中国最普遍的肝脏疾病,随着病程的进展会对身体和健康产生诸多负面影响,如肝功能受损,MAFLD可导致肝炎、肝纤维化,甚至发展为肝硬化及肝癌;MAFLD还可导致身体代谢紊乱,从而影响能量代谢和胰岛素抵抗,诱导糖尿病、高血压和心血管疾病的发生。越来越多的研究显示,线粒体自噬能够降解受损或老化的线粒体,维持生物体内线粒体的数量和质量,在MAFLD的进展中发挥着非常重要的作用。已有研究表明,部分中药和复方可以通过调控线粒体自噬途径来治疗MAFLD。文章对中医药调控线粒体自噬治疗代谢相关脂肪性肝病的机制研究作一综述,为该病今后的防治策略提供参考。

关键词：代谢相关脂肪性肝病线粒体自噬 PINK1/Parkin bnip3 TEFB

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FTO protects human granulosa cells from chemotherapy-induced cytotoxicity

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REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY 2022年第1期20卷 39-39页

作者： Wang, Rongli Wang, Wei Wang, Lijun Yuan, Linnan Cheng, Feiyan Guan, Xin Zheng, Nini Yang, Xinyuan Xi An Jiao Tong Univ Dept Obstet & Gynecol Affiliated Hosp 1 Xian 710061 Peoples R China Xi An Jiao Tong Univ Dept Anesthesiol Affiliated Hosp 1 Xian 710061 Peoples R China

Background Premature ovarian failure (POF) is a serious problem for young women who receive chemotherapy, and its pathophysiological basis is the dysfunction of granulosa cells. According to previous reports, menstrual-derived stem cells (MenSCs) can restore ovarian function and folliculogenesis in mice with chemotherapy-induced POF. Fat mass- and obesity-associated (FTO) was reported to be associated with oocyte development and maturation. FTO was decreased in POF and may be a biomarker for the occurrence of POF. Knockdown of FTO in granulosa cells promoted cell apoptosis and inhibited proliferation. But the relationship between FTO and ovarian repair was still unclear. This study was aimed at investigating the FTO expression level and the role of FTO in the MenSCs recovering the function of injured granulosa cells. Method First, cisplatin was used to establish a granulosa cell injury model. Then, the MenSCs and injured granulosa cell coculture model and POF mouse model were established in this study to explore the role of FTO. Furthermore, gain- and loss-of-function studies, small interfering RNA transfection, and meclofenamic acid (MA), a highly selective inhibitor of FTO, studies were also conducted to clarify the regulatory mechanism of FTO in granulosa cells. Results MenSCs coculture could improve the function of injured granulosa cells by increasing the expression of FTO. MenSCs transplantation restored the expression of FTO in the ovaries of POF mice. Overexpression of FTO restored the injured cell proliferation and decreased apoptosis by regulating the expression of bnip3. Down-regulation of FTO got the opposite results. Conclusions In the treatment of MenSCs, FTO has a protective effect, which could improve the viability of granulosa cells after cisplatin treatment by decreasing the expression of bnip3. Meanwhile, FTO may provide new insight into therapeutic targets for the chemotherapy-induced POF.

关键词： FTO POF Menstrual-derived stem cells bnip3

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Metformin alleviates bone loss in ovariectomized mice through inhibition of autophagy of osteoclast precursors mediated by E2F1

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CELL COMMUNICATION AND SIGNALING 2022年第1期20卷 165-165页

作者： Xie, Xudong Hu, Liangcong Mi, Bobin Xue, Hang Hu, Yiqiang Panayi, Adriana C. Endo, Yori Chen, Lang Yan, Chenchen Lin, Ze Li, Hui Zhou, Wu Liu, Guohui Huazhong Univ Sci & Technol Union Hosp Tongji Med Coll Dept Orthoped Wuhan 430022 Peoples R China Hubei Prov Key Lab Oral & Maxillofacial Dev & Reg Wuhan 430022 Peoples R China Harvard Med Sch Brigham & Womens Hosp Div Plast Surg Boston MA 02215 USA

Background: Postmenopausal bone loss, mainly caused by excessive bone resorption mediated by osteoclasts, has become a global public health burden. Metformin, a hypoglycemic drug, has been reported to have beneficial effects on maintaining bone health. However, the role and underlying mechanism of metformin in ovariectomized (OVX)induced bone loss is still vague. Results: In this study, we demonstrated for the first time that metformin administration alleviated bone loss in postmenopausal women and ovariectomized mice, based on reduced bone resorption markers, increased bone mineral density (BMD) and improvement of bone microstructure. Then, osteoclast precursors administered metformin in vitro and in vivo were collected to examine the differentiation potential and autophagical level. The mechanism was investigated by infection with lentivirus-mediated bnip3 or E2F1 overexpression. We observed a dramatical inhibition of autophagosome synthesis and osteoclast formation and activity. Treatment with RAPA, an autophagy activator, abrogated the metformin-mediated autophagy downregulation and inhibition of osteoclastogenesis. Additionally, overexpression of E2F1 demonstrated that reduction of OVX-upregulated autophagy mediated by metformin was E2F1 dependent. Mechanistically, metformin-mediated downregulation of E2F1 in ovariectomized mice could downregulate BECN1 and bnip3 levels, which subsequently perturbed the binding of BECN1 to BCL2. Furthermore, the disconnect between BECN1 and BCL2 was shown by bnip3 overexpression. Conclusion: In summary, we demonstrated the effect and underlying mechanism of metformin on OVX-induced bone loss, which could be, at least in part, ascribed to its role in downregulating autophagy during osteoclastogenesis via E2F1-dependent BECN1 and BCL2 downregulation, suggesting that metformin or E2F1 inhibitor is a potential agent against postmenopausal bone loss.

关键词： Metformin Osteoclast precursors Bone loss Autophagy E2F1 BECN1 bnip3

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Differential impact of doxorubicin dose on cell death and autophagy pathways during acute cardiotoxicity

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TOXICOLOGY AND APPLIED PHARMACOLOGY 2022年 453卷 116210页

作者： Kawalec, Philip Martens, Matthew D. Field, Jared T. Mughal, Wajihah Caymo, Andrei Miguel Chapman, Donald Xiang, Bo Ghavami, Saeid Dolinsky, Vernon W. Gordon, Joseph W. Univ Manitoba Rady Fac Hlth Sci Dept Human Anat & Cell Sci Winnipeg MB Canada Univ Manitoba Rady Fac Hlth Sci Dept Pharmacol & Therapeut Winnipeg MB Canada Univ Manitoba Coll Nursing Rady Fac Hlth Sci Winnipeg MB Canada Childrens Hosp Res Inst Manitoba Winnipeg MB Canada

Doxorubicin (DOX) is an effective anthracycline used in chemotherapeutic regimens for a variety of haematological and solid tumors. However, its utility remains limited by its well-described, but poorly understood cardiotoxicity. Despite numerous studies describing various forms of regulated cell death and their involvement in DOX-mediated cardiotoxicity, the predominate form of cell death remains unclear. Part of this inconsistency lies in a lack of standardization of in vivo and in vitro model design. To this end, the objective of this study was to characterize acute low- and high-dose DOX exposure on cardiac structure and function in C57BL/6 N mice, and evaluate regulated cell death pathways and autophagy both in vivo and in cardiomyocyte culture models. Acute low-dose DOX had no significant impact on cardiac structure or function;however, acute high-dose DOX elicited substantial cardiac necrosis resulting in diminished cardiac mass and volume, with a corresponding reduced cardiac output, and without impacting ejection fraction or fibrosis. Low-dose DOX consistently activated caspase-signaling with evidence of mitochondrial permeability transition. However, acute high-dose DOX had only modest impact on common necrotic signaling pathways, but instead led to an inhibition in autophagic flux. Intriguingly, when autophagy was inhibited in cultured cardiomyoblasts, DOX-induced necrosis was enhanced. Collectively, these observations implicate inhibition of autophagy flux as an important component of the acute necrotic response to DOX, but also suggest that acute high-dose DOX exposure does not recapitulate the disease phenotype observed in human cardiotoxicity.

关键词： Doxorubicin Cardiotoxicity Cell death Autophagy bnip3

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