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Genes & Diseases 2022年第6期9卷 1419-1422页

作者： Francisco Gallardo-Chamizo Nieves Lara-Urena Juan F.Correa-Vazquez Jose C.Reyes Benoit R.Gauthier Mario Garcia-Dominguez Cell Dynamics and Signaling Department CABIMERCSICUniversidad de Sevilla-Universidad Pablo de Olavide-Junta de AndaluciaSeville 41092Spain Genome Biology Department CABIMERCSIC-Universidad de Sevilla-Universidad Pablo de Olavide-Junta de AndaluciaSeville 41092Spain Cell Therapy and Regeneration Department CABIMERCSIC-Universidad de Sevilla-Universidad Pablo de Olavide-Junta de AndaluciaSeville 41092Spain Centro de Investigacion Biomedica en Red de Diabetes y Enfermedades Metabo´licas Asociadas(CIBERDEM) Madrid 28029Spain

To the Editor,Constricted oxygen and glucose supplies are common conditions that healthy cells following a stress such an ischemic insult as well as cancer cells within a solid tumor need to overcome in order to survive.These conditions are a serious challenge for cells,which accurately measure the impact to make a life or death decision.In cancer cells,aberrant gene expression and/or protein regulation,frequently linked to appearing mutations,may confer selective advantages to survive under these adverse conditions.In the past years,cumulative evidence indicates that protein modification by covalent attachment of the Small Ubiquitin-like MOdifier(SUMO)plays a role in cell survival after oxygen and glucose deprivation(OGD).

关键词： cancer deprivation colon

SEMA3A-mediated crosstalk between prostate cancer cells and tumor-associated macrophages promotes androgen deprivation therapy resistance

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Cellular & Molecular Immunology 2021年第3期18卷 752-754页

作者： Fei Liu Chao Wang Hai Huang Yue Yang Lihe Dai Sujun Han Nianzeng Xing Shancheng Ren Department of Urology Shanghai Changhai HospitalShanghaiChina Department of Urology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina State Key Laboratory of Kidney Diseases BeijingChina Department of Urinary Surgery Gongli Hospitalthe Second Military Medical UniversityShanghaiChina Department of Urinary Surgery Ruijin HospitalShanghai Jiao tong University School of MedicineShanghaiChina

Androgen deprivation therapy(ADT)is an important treatment strategy that can be used to delay the progression of prostate cancer.However,after an initial response,which varies significantly among patients,the disease eventually progresses despite the low levels of testosterone in the systemic circulation.1 The mechanism underlying the progression of prostate cancer to castration-resistant prostate cancer(CRPC)is not yet clear,and further investigation is needed.

关键词： cancer deprivation therapy

Silencing Huwe1 reduces apoptosis of cortical neurons exposed to oxygen-glucose deprivation and reperfusion

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Neural Regeneration Research 2019年第11期14卷 1977-1985页

作者： Guo-Qian He Wen-Ming Xu Hui-Juan Liao Chuan Jiang Chang-Qing Li Wei Zhang Department of Pediatrics Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University)Ministry of EducationWest China Second University HospitalSichuan UniversityChengduSichuan ProvinceChina Joint Laboratory of Reproductive Medicine Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University)Ministry of EducationWest China Second University HospitalSichuan UniversityChengduSichuan ProvinceChina Department of Neurology The Second Affiliated Hospital of Chongqing Medical UniversityChongqingChina Department of Medical Oncology Sichuan Cancer Hospital & InstituteSichuan Cancer CenterCancer Hospital Affiliated to School of MedicineUniversity of Electronic Science and Technology of ChinaChengduSichuan ProvinceChina

HECT, UBA and WWE domain-containing 1(Huwe1), an E3 ubiquitin ligase involved in the ubiquitin-proteasome system, is widely expressed in brain tissue. Huwe1 is involved in the turnover of numerous substrates, including p53, Mcl-1, Cdc6 and N-myc, thereby playing a critical role in apoptosis and neurogenesis. However, the role of Huwe1 in brain ischemia and reperfusion injury remains unclear. Therefore, in this study, we investigated the role of Huwe1 in an in vitro model of ischemia and reperfusion injury. At 3 days in vitro, primary cortical neurons were transduced with a control or shRNA-Huwe1 lentiviral vector to silence expression of Huwe1. At 7 days in vitro, the cells were exposed to oxygen-glucose deprivation for 3 hours and reperfusion for 24 hours. To examine the role of the c-Jun N-terminal kinase(JNK)/p38 pathway, cortical neurons were pretreated with a JNK inhibitor(SP600125) or a p38 MAPK inhibitor(SB203508) for 30 minutes at 7 days in vitro, followed by ischemia and reperfusion. Neuronal apoptosis was assessed by TUNEL assay. Protein expression levels of JNK and p38 MAPK and of apoptosis-related proteins(p53, Gadd45 a, cleaved caspase-3, Bax and Bcl-2) were measured by western blot assay. Immunofluorescence labeling for cleaved caspase-3 was performed. We observed a significant increase in neuronal apoptosis and Huwe1 expression after ischemia and reperfusion. Treatment with the shRNA-Huwe1 lentiviral vector markedly decreased Huwe1 levels, and significantly decreased the number of TUNEL-positive cells after ischemia and reperfusion. The silencing vector also downregulated the pro-apoptotic proteins Bax and cleaved caspase-3, and upregulated the anti-apoptotic proteins Gadd45 a and Bcl-2. Silencing Huwe1 also significantly reduced p-JNK levels and increased p-p38 levels. Our findings show that downregulating Huwe1 affects the JNK and p38 MAPK signaling pathways as well as the expression of apoptosis-related genes to provide neuroprotection during ischemia and reperfusion. All animal experiments and

关键词： nerve regeneration ischemic stroke oxygen-glucose deprivation and reperfusion ischemia/reperfusion cortical neuron ubiquitin proteasome system Huwe1 apoptosis therapeutic targets cell culture cell death neural regeneration

Knocking down TRPM2 expression reduces cell injury and NLRP3 inflammasome activation in PC12 cells subjected to oxygen-glucose deprivation

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Neural Regeneration Research 2020年第11期15卷 2154-2161页

作者： Tao Pan Qiu-Jiao Zhu Li-Xiao Xu Xin Ding Jian-Qin Li Bin Sun Jun Hua Xing Feng Department of Neonatology Children’s Hospital Affiliated to Suzhou UniversitySuzhouJiangsu ProvinceChina Department of Critical Care Medicine Children’s Hospital Affiliated to Suzhou UniversitySuzhouJiangsu ProvinceChina Institute of Pediatrics Children’s Hospital Affiliated to Suzhou UniversitySuzhouJiangsu ProvinceChina Blood Section Children’s Hospital Affiliated to Suzhou UniversitySuzhouJiangsu ProvinceChina

Transient receptor potential melastatin 2(TRPM2) is an important ion channel that represents a potential target for treating injury caused by cerebral ischemia. However, it is unclear whether reducing TRPM2 expression can help repair cerebral injury, and if so what the mechanism underlying this process involves. This study investigated the protective effect of reducing TRPM2 expression on pheochromocytoma(PC12) cells injured by oxygen-glucose deprivation(OGD). PC12 cells were transfected with plasmid encoding TRPM2 shRNAS, then subjected to OGD by incubation in glucose-free medium under hypoxic conditions for 8 hours, after which the cells were allowed to reoxygenate for 24 hours. Apoptotic cells, mitochondrial membrane potentials, reactive oxygen species levels, and cellular calcium levels were detected using flow cytometry. The relative expression of C-X-C motif chemokine ligand 2(CXCL2), NACHT, LRR, and PYD domain–containing protein 3(NALP3), and caspase-1 were detected using fluorescence-based quantitative reverse transcription-polymerase chain reaction and western blotting. The rates of apoptosis, mitochondrial membrane potentials, reactive oxygen species levels, and cellular calcium levels in the TRPM2-shRNA + OGD group were lower than those observed in the OGD group. Taken together, these results suggest that TRPM2 knockdown reduces OGD-induced neuronal injury, potentially by inhibiting apoptosis and reducing oxidative stress levels, mitochondrial membrane potentials, intracellular calcium concentrations, and NLRP3 inflammasome activation.

关键词： apoptosis calcium caspase-1 NLRP3 mitochondrial impairment oxidative stress oxygen-glucose deprivation PC12 shRNA TRPM2

Hyodeoxycholic acid protects the neurovascular unit against oxygen-glucose deprivation and reoxygenation-induced injury in vitro

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Neural Regeneration Research 2019年第11期14卷 1941-1949页

作者： Chang-Xiang Li Xue-Qian Wang Fa-Feng Cheng Xin Yan Juan Luo Qing-Guo Wang School of Traditional Chinese Medicine Beijing University of Chinese Medicine

Calculus bovis is commonly used for the treatment of stroke in traditional Chinese medicine. Hyodeoxycholic acid(HDCA) is a bioactive compound extracted from calculus bovis. When combined with cholic acid, baicalin and jas-minoidin, HDCA prevents hypoxia-reoxygenation-induced brain injury by suppressing endoplasmic reticulum stress-mediated apoptotic signaling. However, the effects of HDCA in ischemic stroke injury have not yet been studied. Neurovascular unit(NVU) dysfunction occurs in ischemic stroke. Therefore, in this study, we investigated the effects of HDCA on the NVU under ischemic conditions in vitro. We co-cultured primary brain microvascular endothelial cells, neurons and astrocytes using a transwell chamber co-culture system. The NVU was pre-treated with 10.16 or 2.54 μg/mL HDCA for 24 hours before exposure to oxygen-glucose deprivation for 1 hour. The cell counting kit-8 assay was used to detect cell activity. Flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling were used to assess apoptosis. Enzyme-linked immunosorbent assay was used to measure the expression levels of inflammatory cytokines, including interleukin-1β, interleukin-6 and tumor necrosis factor-α, and neurotrophic factors, including brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor. Oxidative stress-related factors, such as superoxide dismutase, nitric oxide, malondialdehyde and γ-glutamyltransferase, were measured using kits. Pretreatment with HDCA significantly decreased blood-brain barrier permeability and neuronal apoptosis, significantly increased transendothelial electrical resistance and γ-glutamyltransferase activity, attenuated oxidative stress damage and the release of inflammatory cytokines, and increased brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor expression. Our findings suggest that HDCA maintains NVU morphological integrity and function by modulating inflammation, oxidation stress, apoptosis, and the expression of neu

关键词： hyodeoxycholic acid oxygen glucose deprivation and reoxygenation blood-brain barrier permeability anti-oxidative anti-inflammatory anti-apoptotic brain-derived neurotrophic factor glial cell line-derived neurotrophic factor ischemic stroke in vitro neurovascular unit

Ethanol exposed maturing rat cerebellar granule cells show impaired energy metabolism and increased cell death after oxygen-glucose deprivation

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Neural Regeneration Research 2019年第3期14卷 485-490页

作者： Ana Spataru Diana Le Duc Leon Zagrean Ana-Maria Zagrean Division of Physiology and Neuroscience Carol Davila University of Medicine and Pharmacy King's College Hospital London UK Institute of Human Genetics University of Leipzig Hospitals and Clinics Leipzig GermanyDepartment of Evolutionary Genetics Max Planck Institute for Evolutionary Anthropology

Alcohol, a widely abused drug, has deleterious effects on the immature nervous system. This study investigates the effect of chronic in vitro ethanol exposure on the metabolism of immature rat cerebellar granular cells(CGCs) and on their response to oxygen-glucose deprivation(OGD). Primary CGC cultures were exposed to ethanol(100 mM in culture medium) or to control ethanol-free medium starting day one in vitro(DIV1). At DIV8, the expression of ATP synthase gene ATP5 g3 was quantified using real-time PCR, then cultures were exposed to 3 hours of OGD or normoxic conditions. Subsequently, cellular metabolism was assessed by a resazurin assay and by ATP level measurement. ATP5 g3 expression was reduced by 12-fold(P = 0.03) and resazurin metabolism and ATP level were decreased to 74.4 ± 4.6% and 55.5 ± 6.9%, respectively after chronic ethanol treatment compared to control values(P deprivation. Thus, interventions which improve metabolic function and sustain ATP-levels could attenuate ethanol-induced neuronal dysfunction and should be addressed in future studies.

关键词： cell culture chronic ethanol exposure oxygen-glucose deprivation cerebellar granule cells toxicity gene expression cellular ATP cellular metabolism metabolic impairment cell death

ROS is essential for initiation of energy deprivation-induced autophagy

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Journal of Genetics and Genomics 2021年第6期48卷 512-515页

作者： Choufei Wu Yixing Li Shu Zhong Yingcong Chen Yu Xie Yuyao Feng Weijing Yao Suping Fu Yanlan Zhu Liefeng Wang Yuting Chen Liqin Zhang Jingjing Tong Cong Yi Key Laboratory of Vector Biology and Pathogen Control of Zhejiang Province School of Life SciencesHuzhou UniversityHuzhou 313000China Department of Biochemistry and Department of Hepatobiliary and Pancreatic Surgery of the First Affiliated HospitalZhejiang University School of MedicineHangzhou 310058China School of Life Sciences Central China Normal UniversityWuhan 430079China College of Chemistry and Bio-Engineering Yichun UniversityYichun 336000China Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases of Ministry of Education Gannan Medical UniversityGanzhou 341000China

Autophagy is a highly conserved degradation process in which intracellular components are engulfed into a double membrane structure,known as the autophagosomes,and then delivered to lysosomes/vacuoles for degradation(Ohsumi,2014).Recently,autophagy has been found to be responsible for maintaining glucose homeostasis in adult animals(Karsli-Uzunbas et al.,2014).However,the molecular mechanism underlying energy deprivation-induced autophagy remains relatively unclear.

关键词： deprivation homeostasis

Proprotein convertase 1/3-mediated down-regulation of brain-derived neurotrophic factor in cortical neurons induced by oxygen-glucose deprivation

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Neural Regeneration Research 2020年第6期15卷 1066-1070页

作者： Xiang-Yang Zhang Feng Liu Yan Chen Wei-Chun Guo Zhao-Hui Zhang Department of Orthopedics Renmin Hospital of Wuhan UniversityWuhanHubei ProvinceChina Department of Neurology Renmin Hospital of Wuhan UniversityWuhanHubei ProvinceChina

Brain-derived neurotrophic factor(BDNF)has robust effects on synaptogenesis,neuronal differentiation and synaptic transmission and plasticity.The maturation of BDNF is a complex process.Proprotein convertase 1/3(PC1/3)has a key role in the cleavage of protein precursors that are directed to regulated secretory pathways;however,it is not clear whether PC1/3 mediates the change in BDNF levels caused by ischemia.To clarify the role of PC1/3 in BDNF maturation in ischemic cortical neurons,primary cortical neurons from fetal rats were cultured in a humidified environment of 95%N_2 and 5%CO_2 in a glucose-free Dulbecco's modified Eagle's medium at 37℃for3 hours.Enzyme-linked immunosorbent assays and western blotting showed that after oxygen-glucose deprivation,the secreted and intracellular levels of BDNF were significantly reduced and the intracellular level of PC1/3 was decreased.Transient transfection of cortical neurons with a PC1/3 overexpression plasmid followed by oxygen-glucose deprivation resulted in increased PC1/3 levels and increased BDNF levels.When levels of the BDNF precursor protein were reduced,the concentration of BDNF in the culture medium was increased.These results indicate that PC 1/3 cleavage of BDNF is critical for the conversion of pro-BDNF in rat cortical neurons during ischemia.The study was approved by the Animal Ethics Committee of Wuhan University School of Basic Medical Sciences.

关键词： cortical neuron ischemia neurotrophin oxygen-glucose deprivation precursor protein of brain-derived neurotrophic factor proprotein convertase proprotein convertase 1/3

Auditory deprivation modifies the expression of brain-derived neurotrophic factor and tropomyosin receptor kinase B in the rat auditory cortex

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Journal of Otology 2017年第1期12卷 34-40页

作者： Yuxing Wang Ou Xu Yanxing Liu Hong Lu Department of Otorhinolaryngology The Second Hospital of Hebei Medical University Department of Pharmacology Hebei Medical University

The development and plasticity of central auditory system can be influenced by the change of peripheral neuronal activity. However, the molecular mechanism participating in the process remains elusive. Brain-derived neurotrophic factor(BDNF) binding with its functional receptor tropomyosin receptor kinase B(TrkB) has multiple effects on neurons. Here we used a rat model of auditory deprivation by bilateral cochlear ablation, to investigate the changes in expression of BDNF and Trk B in the auditory cortex after auditory deprivation that occurred during the critical period for the development of central auditory system. Reverse transcription-quantitative polymerase chain reaction(RTqPCR) and immunohistochemistry methods were adopted to detect the m RNA and protein expression levels of BDNF and TrkB in the auditory cortex at 2, 4, 6 and 8 weeks after surgery, respectively. The change in the expression of BDNF and TrkB mRNAs and proteins followed similar trend. In the bilateral cochlear ablation groups, the BDNF-TrkB expression level initially decreased at 2 weeks but increased at 4 weeks followed by the reduction at 6 and 8 weeks after cochlear removal, as compared to the age-matched sham control groups. In conclusion, the BDNF-TrkB signaling is involved in the plasticity of auditory cortex in an activity-dependent manner.

关键词： Central plasticity Brain-derived neurotrophic factor Tropomyosin receptor kinase B Auditory deprivation Auditory cortex

Effects of Exercise on Cancer-related Fatigue and Quality of Life in Prostate Cancer Patients Undergoing Androgen deprivation Therapy: A Meta-analysis of Randomized Clinical Trials

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Chinese Medical Sciences Journal 2017年第1期32卷 13-21页

作者： Bo Yang Jiansheng Wang Department of Urology Xixi Hospital of Hangzhou Hangzhou 310023 China

Objective To gain insight on how exercise affects the outcomes of prostate cancer patients treated with androgen deprivation therapy,specifically cancer-related fatigue(CRF) and quality of life(QoL). Methods Systematic searches for randomized clinical trials(RCTs) evaluating the effects of exercise on CRF and QoL of prostate cancer patients receiving androgen deprivation therapy were carried out to identify the eligible studies from EMBASE,Pub Med and Cochrane library. Related data were extracted from eligible studies and then subjected to Reviewer Manage 5.3 for analysis. Standardized mean differences(SMD) and its 95% confidence interval(CI) were calculated. Results In all,10 RCTs involving 841 prostate cancer patients(448 of whom exercised and 393 did not) were included in this study. With respect to CRF,there was good consistency among different studies,and it was remarkably reduced in the exercise group(SMD=-0.32,95% CI:-0.45 to-0.18,Pdeprivation therapy.

关键词： exercise cancer related fatigue prostate cancer androgen deprivation therapy meta-analysis