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BDNF Overexpression Enhances the Preconditioning Effect of Brief Episodes of Hypoxia,Promoting Survival of GABAergic Neurons

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Neuroscience Bulletin 2020年第7期36卷 733-760页

作者： M.V.Turovskaya S.G.Gaidin M.V.Vedunova A.A.Babaev E.A.Turovsky Institute of Cell Biophysics of the Russian Academy of Sciences Federal Research Center“Pushchino Scientific Center for Biological Research of the Russian Academy of Sciences”PushchinoRussia Institute of Biology and Biomedicine Lobachevsky State University of Nizhny NovgorodNizhny NovgorodRussia

Hypoxia causes depression of synaptic plasticity,hyperexcitation of neuronal networks,and the death of specific populations of neurons.However,brief episodes of hypoxia can promote the adaptation of cells.Hypoxic Preconditioning is well manifested in glutamatergic neurons,while this adaptive mechanism is virtually suppressed in GABAergic neurons.Here,we show that brain-derived neurotrophic factor(BDNF) overexpression in neurons enhances the Preconditioning effect of brief episodes of hypoxia.The amplitudes of the NMDAR-and AMPARmediated Ca2+ responses of glutamatergic and GABAergic neurons gradually decreased after repetitive brief hypoxia/reoxygenation cycles in cell cultures transduced with the(AAV)-Syn-BDNF-EGFP virus construct.In contrast,the amplitudes of the responses of GABAergic neurons increased in non-transduced cultures after Preconditioning.The decrease of the amplitudes in GABAergic neurons indicated the activation of mechanisms of hypoxic Preconditioning.Preconditioning suppressed apoptotic or necrotic cell death.This effect was most pronounced in cultures with BDNF overe xpression.Knockdown of BDNF abolished the effect of Preconditioning and promoted the death of GABAergic neurons.Moreover,the expression of the anti-apoptotic genes Stat3,Socs3,and Bcl-x1 substantially increased 24 h after hypoxic episodes in the transduced cultures compared to controls.The expression of genes encoding the pro-inflammatory cytokines IL-10 and IL-6 also increased.In turn,the expression of pro-apoptotic(Bax,Casp-3,and Fas) and proinflammatory(IL-1β and TNFα) genes decreased after hypoxic episodes in cultures with BDNF overexpression.Inhibition of vesicular BDNF release abolished its protective action targeting inhibition of the oxygen-glucose deprivation(OGD)-induced [Ca2+]i increase in GABAergic and glutamatergic neurons,thus promoting their death.Bafilomycin A1,Brefeldin A,and tetanus toxin suppressed vesicular release(including BDNF) and shifted the gene expression profile towards excitotoxicity,inflammation,and ap

关键词： Hypoxia Neuron BDNF Preconditioning Calcium Receptors

An overview of ischemic Preconditioning in exercise performance:A systematic review

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Journal of Sport and Health Science 2019年第4期8卷 355-369页

作者： Maxime Caru Ariane Levesque Francois Lalonde Daniel Cumier Laboratory of Pathophysiology of EXercise(LPEX) School of Kinesiology and Physical Activity SciencesFaculty of MedicineUniversity of MontrealMontrealQuebec H3T1J4Canada Department of Psychology University of Paris-NanterreNanterre 92000France Laboratoire EA 4430-Clinique Psychanalyse Developpement(CliPsyD) University of Paris-NanterreNanterre 92000France CHUSte-Justine Research Center CHUSte-JustineMontreal H3T1C5Canada Department of Psychology McGill UniversityMontrealQuebec H3A 1G1Canada Department of Physical Activity Sciences Faculty of SciencesUniversite du Quebec a MontrealMontrealQuebec H2L 2C4Canada

Ischemic Preconditioning(IPC)is an attractive method for athletes owing to its potential to enhance exercise performance.However,the effectiveness of the IPC intervention in the field of sports science remains mitigated.The number of cycles of ischemia and reperfusion,as well as the duration of the cycle,varies from one study to another;Thus,the aim of this systematic review was to provide a comprehensive review examining the IPC literature in sports science.A systematic literature search was performed in PubMed(MEDLINE)(from 1946 to May 2018),Web of Science(sport sciences)(from 1945 to May 2018),and EMBASE(from 1974 to May 2018).We included all studies investigating the effects of IPC on exercise performance in human subjects.To assess scientific evidence for each study,this review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement.The electronic database search generated 441 potential articles that were screened for eligibility.A total of 52 studies were identified as eligible and valid for this systematic review.The studies included were of high quality,with 48 of the 52 studies having a ran?domized,controlled trial design.Most studied showed that IPC intervention can be beneficial to exercise performance.However,IPC intervention seems to be more beneficial to healthy subjects who wish to enhance their performance in aerobic exercises than athletes.Thus,this systematic review highlights that a better knowledge of the mechanisms generated by the IPC intervention would make it possible to optimize the protocols according to the characteristics of the subjects with the aim of suggesting to the subjects the best possible experience of IPC intervention.

关键词： Exercise Human performance IPC protocols Ischemic Preconditioning Sports science

Poly(I:C)Preconditioning protects the heart against myocardial ischemia/reperfusion injury through TLR3/PI3K/Akt-dependent pathway

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Signal Transduction and Targeted Therapy 2020年第1期5卷 264-278页

作者： Erya Chen Chan Chen Zhendong Niu Lu Gan Qiao Wang Ming Li XingWei Cai Rui Gao Sruthi Katakam Hai Chen Shu Zhang Ronghua Zhou Xu Cheng Yanhua Qiu Hai Yu Tao Zhu Jin Liu Department of Anesthesiology and Translational Neuroscience Center West China HospitalSichuan UniversityChengduSichuanChina Department of Emergency Medicine West China HospitalSichuan UniversityChengduSichuanChina Institute of Cell Engineering Department of NeurologySchool of MedicineJohns Hopkins UniversityBaltimoreMDUSA

Emerging evidence suggests that Toll-like receptors(TLRs)ligands pretreatment may play a vital role in the progress of myocardial ischemia/reperfusion(I/R)injury.As the ligand of TLR3,polyinosinic-polycytidylic acid(poly(I:C)),a synthetic double-stranded RNA,whether its Preconditioning can exhibit a cardioprotective phenotype remains unknown.Here,we report the protective effect of poly(I:C)pretreatment in acute myocardial I/R injury by activating TLR3/PI3K/Akt signaling pathway.Poly(I:C)pretreatment leads to a significant reduction of infarct size,improvement of cardiac function,and downregulation of inflammatory cytokines and apoptotic molecules compared with controls.Subsequently,our data demonstrate that phosphorylation of TLR3 tyrosine residue and its interaction with PI3K is enhanced,and protein levels of phospho-PI3K and phospho-Akt are both increased after poly(I:C)pretreatment,while knock out of TLR3 suppresses the cardioprotection of poly(I:C)Preconditioning through a decreased activation of PI3K/Akt signaling.Moreover,inhibition of p85 PI3K by the administration of LY294002 in vivo and knockdown of Akt by siRNA in vitro significantly abolish poly(I:C)Preconditioning-induced cardioprotective effect.In conclusion,our results reveal that poly(I:C)Preconditioning exhibits essential protection in myocardial I/R injury via its modulation of TLR3,and the downstream PI3K/Akt signaling,which may provide a potential pharmacologic target for perioperative cardioprotection.

关键词： PI3K/Akt protective Preconditioning

Effects of volatile anesthetic Preconditioning on expression of NFkB-regulated genes in aged rat myocardium

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The Journal of Biomedical Research 2019年第4期33卷 264-270页

作者： Caiyun Zhong Hong Qiu Jun Chen Hong Liu School of Public Health Nanjing Medical UniversityNanjingJiangsu 211166China Department of Pathology University of California Davis HealthSacramentoCA 95817USA Department of Anesthesiology the First Affiliated Hospital ofSoochow UniversitySuzhouJiangsu 215006China Department of Anesthesiology and Pain Medicine University of California Davis HealthSacramentoCA 95817USA.

Volatile anesthetic Preconditioning has been shown to be a potent way to provide myocardium protection against ischemia/reperfusion(I/R)injury;however,this cardioprotection is lost in senescent animal models and elderly patients.NFκB-regulated genes have been linked to myocardial I/R injury and anesthetic Preconditioning.Here,we investigated NFκB activation related to anesthetic Preconditioning in aging rat myocardium.Isolated,Langendorff perfused rat hearts from Fischer 344 male rats,24 months old,were randomly assigned to one of the three groups.The hearts of the control group were perfused with physiologic solution without any intervention.The hearts in the I/R group were subjected to 25 minutes ischemia and followed by 60 minutes reperfusion.The hearts in the treatment group were subjected to 10 minutes 2.5% sevoflurane,followed by 20 minutes washout and by 25 minutes ischemia and 60 minutes of reperfusion,respectively.Left ventricular developed pressure(LVDP)and left ventricular enddiastolic pressure(LVEDP)were measured.Western blot analysis was used to measure inhibitor of κB(IκB)and antiapoptotic genes:A1,ILP,c-IAP-2,Bcl-2,caspase 8 and caspase 9.Ischemia and reperfusion significantly decreased LVDP and increased LVEDP in aged rat hearts.Anesthetic Preconditioning with sevoflurane did not change the effects I/R on LVDP and LVEDP,despite the fact that after treatment with anesthetic Preconditioning,the levels of IκB,A1,ILP,caspase 8 and caspase 9 were significantly different compared to those of the control hearts.In conclusion,anesthetic Preconditioning with sevoflurane does not improve myocardial systolic and diastolic functions.Our results suggest that the activation of NFκB regulated genes is different in the senescent myocardium and could account for loss of cardioprotection with aging.

关键词： aging inflammatory apoptosis anesthesia Preconditioning

Expression profile of circular RNAs in myocardial ischemia/reperfusion with and without intermittent hypobaric hypoxia Preconditioning

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Science China(Life Sciences) 2019年第8期62卷 1104-1106页

作者： Jiliang Tan Shanshan Gu Yanjun Zheng Huangtian Yang CAS Key Laboratory of Tissue Microenvironment and Tumor Laboratory of Molecular CardiologyShanghai Institute of Nutrition and HealthShanghai Institutes for Biological SciencesChinese Academy of SciencesShanghai200031China Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijing100101China

Dear Editor,Myocardial injury following ischemia/reperfusion(I/R)is a common clinical scenario in patients suffering from ischemic heart disease(Hausenloy et al.,2016).The involvement of proteins and signaling pathways is well studied in myocardial I/R injury and protection(Hausenloy et al.,2016;Yang et al.,2012),however,more than 98%of the transcriptional output in mammals are noncoding RNAs(ncRNAs).These products range from short microRNAs(miRNAs)to long noncoding RNAs(lncRNAs,Das et al.,2018)and modulate critical pathophysiologic mechanisms,such as apoptosis,oxidative stress,Ca2+overload and inflammation,during myocardial I/R injury and protection(Das et al.,2018).

关键词： circRNA Expression profile of circular RNAs in myocardial ischemia/reperfusion with and without intermittent hypobaric hypoxia Preconditioning profile

Wnt/Glycogen Synthase Kinase 3β/β-catenin Signaling Activation Mediated Sevoflurane Preconditioning-induced Cardioprotection

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Chinese Medical Journal 2015年第17期128卷 2346-2353页

作者： Jin-Dong Liu Qian Deng Huan-Huan Tian Yun-Ting Pang Gan-Lin Deng Department of Anesthesiology The Affiliated Hospital of Xuzhou Medical College Jiangsu Province Key Laboratory of Anesthesiology Xuzhou Medical College Xuzhou Jiangsu 221004 China Jiangsu Province Key Laboratory of Anesthesiology Xuzhou Medical College Xuzhou Jiangsu 221004 China

Background： Sevoflurane Preconditioning （SP） has been shown to invoke potent myocardial protection in animal studies and clinical trials. However, the mechanisms underlying SP are complex and not yet well understood. We investigated the hypothesis that the cardioprotection afforded by SP is mediated via the Writ/glycogen synthase kinase 3β（GSK3β）/β-catenin signaling pathway. Methods： Two models were established： A Langendorffperfused rat heart model and the H9C2 cell hypoxia/reoxygenation model. Both rats and H9C2 cells were randomly divided into 6 groups as follows： S group, ischemia-reperfusion （I/R） group, DMSO group, IWP group, SP group, and SP ＋ IWP group. Hemodynamic parameters, lactate dehydrogenase （LDH） activity in coronary effluent and cell culture supernatant, and the infarct size were measured to evaluate myocardial ischemia-reperfusion injuries. To determine the activity of Wnt/GSK3β/β-catenin signaling pathway, the expressions of Wnt3a, phospho-GSK3β, and β-catenin were measured by Western blotting. Results： SP improved cardiac function recovery, reduced infarct size （18 ±2% in the SP group compared with 35 ± 4% in the 1/R group; P 〈 0.05）, decreased LDH activity in coronary effluent, and culture supematant. IWP-2, an inhibitor of Wnt, abolished the cardioprotection by SR In addition, Western blotting analysis demonstrated that the expressions of Wnt3a, phospho-GSK3β, and β-catenin significantly （P 〈 0.05） increased in the I/R group, compared with the S group; and compared to I/R group, SP significantly （P 〈 0.05） increased Wnt3a, phospho-GSK3 β, and β-catenin expressions. Pretreatment with IWP-2 significantly （P 〈 0.05） abolished SP-induced Wnt/GSK3β/β-catenin signaling activation. Conclusions： The results showed for the first time that cardioprotection afforded by SP may be mediated partly via the Wnt/GSK3β/β-catenin signaling pathway.

关键词： Cardioprotection Ischemia-reperfusion Injury Preconditioning Sevoflurane Wnt/Glycogen Synthase Kinase3β/β-catenin Signaling

Inhibitory Effect of Tetramethylpyrazine Preconditioning on Overload Training-Induced Myocardial Apoptosis in Rats

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Chinese Journal of Integrative Medicine 2015年第6期21卷 423-430页

作者：杨翼李章华柳华石武谛张杰 College of Health Science Wuhan Institute of Physical Education Renmin Hospital Wuhan University Graduate Department Wuhan Institute of Physical Education

Objective： To investigate the inhibitory effect of tetramethylpyrazine （Tot） Preconditioning on overload training-induced myocardial apoptosis in rats, and to explore cardioprotective mechanisms of Tot Preconditioning. Methods： A total of 25 male Sprague-Dawley rats were randomly divided into three groups, including the control group （n=5）, the ovedoad training group （overload training for 8 weeks, n=10）, and the Tet Preconditioning group （Tet Preconditioning for 8 weeks before overload training, n=10）. After 8 weeks, cardiac structure and myocardial apoptosis were analyzed by histology, transmission electron microscopy, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay staining. The expressions of Bcl-2, Bax, Caspase-3, and Caspase-9 in myocardium were evaluated by immunohistochemical staining. Results： Overload training caused swelling, disorder, partial rupture, and necrosis of myocardial focal necrotic fibers, as well as mitochondrial vacuolization, cristae rupturing, and blurring. In contrast, Tet Preconditioning attenuated the swelling of myocardial fibers, decreased the amount of ruptured fibers, and inhibited mitochondrial vacuolization, resulting in clear cristae. Overload training significantly increased Bax expression and decreased Bcl-2/Bax ratio when compared with the control group （P〈0.01）. Conversely, Tot Preconditioning significantly increased Bcl-2 expression and the Bcl-2/Bax ratio as compared with the overload training group （P〈0.05）. Overload training dramatically increased the expressions of Caspase-3 and Caspase-9 when compared with the control group （P〈0.05）. Following Tot Preconditioning, the expression of Caspase-3 was significantly reduced compared with the overload training group （P〈0.05）, while Caspase-9 expression showed a slight decline （P〉0.05）. Conclusion： let Preconditioning increased the expression of Bcl-2 and reduced the expression of Caspase-3, thereby attenuating overload training-induced myocardial apoptosis, protecting against overload t

关键词： overload training tetramethylpyrazine Preconditioning myocardial apoptosis

Cellular Preconditioning and mesenchymal stem cell ferroptosis

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World Journal of Stem Cells 2024年第2期16卷 64-69页

作者： Doaa Hussein Zineldeen Mazhar Mushtaq Khawaja Husnain Haider Basic Sciences Sulaiman AlRajhi UniversityAlbukairiyah 52736AlQaseemSaudi Arabia Department of Medical Biochemistry and Molecular Biology Faculty of MedicineTanta UniversityTanta 6632110Egypt

In this editorial,we comment on the article published in the recent issue of the World Journal of Stem Cells.They focus on stem cell Preconditioning to prevent ferroptosis by modulating the cystathionineγ-lyase/hydrogen sulfide(H_(2)S)pathway as a novel approach to treat vascular disorders,particularly pulmonary hypertension.Preconditioned stem cells are gaining popularity in regenerative medicine due to their unique ability to survive by resisting the harsh,unfavorable microenvironment of the injured tissue.They also secrete various paracrine factors against apoptosis,necrosis,and ferroptosis to enhance cell survival.Ferroptosis,a regulated form of cell death characterized by iron accumulation and oxidative stress,has been implicated in various pathologies encompassing dege-nerative disorders to cancer.The lipid peroxidation cascade initiates and sustains ferroptosis,generating many reactive oxygen species that attack and damage multiple cellular structures.Understanding these intertwined mechanisms provi-des significant insights into developing therapeutic modalities for ferroptosis-related diseases.This editorial primarily discusses stem cell Preconditioning in modulating ferroptosis,focusing on the cystathionase gamma/H_(2)S ferroptosis pathway.Ferroptosis presents a significant challenge in mesenchymal stem cell(MSC)-based therapies;hence,the emerging role of H_(2)S/cystathionase gamma/H_(2) S signaling in abrogating ferroptosis provides a novel option for therapeutic intervention.Further research into understanding the precise mechanisms of H_(2)S-mediated cytoprotection against ferroptosis is warranted to enhance the thera-peutic potential of MSCs in clinical settings,particularly vascular disorders.

关键词： Cell survival Cell therapy Hydrogen sulfide Ferroptosis Preconditioning Stem cells Umbilical cord

Late cardioprotection of exercise Preconditioning against exhaustive exercise-induced myocardial injury by up-regulatation of connexin 43 expression in rat hearts

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Asian Pacific Journal of Tropical Medicine 2015年第8期8卷 646-651页

作者： Kai Wang Bai-Chao Xu Hai-Yun Duan Hua Zhang Fu-Song Hu College of Sports Science Qufu Normal University Department of Physical Education Hainan Medical University QiongZhou University Physical Test Room

Objective: To investigate the expression of myocardium connexin 43(Cx43) in late exercise Preconditioning(LEP) cardioprotection. Methods: Eight-week-old adult male Sprague Dawley rats were randomly assigned into four groups(n=8). Myocardial injury was judged in accordance with serum levels of c Tn and NT-pro BNP as well as hematoxylin basicfuchsin picric acid staining of myocardium. Cx43 m RNA was detected by in situ hybridization and qualified by real-time fluorescence quantitative PCR. Cx43 protein was localized by immunohistochemistry and its expression level was determined by western blotting. Results: The LEP obviously attenuated the myocardial ischemia/hypoxia injury caused by exhaustive exercise. There was no significant difference of Cx43 m RNA level between the four groups. Cx43 protein level was decreased significantly in group EE(P<0.05). However, LEP produced a significant increase in Cx43 protein level(P<0.05), and the decreased Cx43 protein level in exhaustive exercise was significantly up-regulated by LEP(P<0.05). Conclusions: LEP protects rat heart against exhaustive exercise-induced myocardial injury by up-regulating the expression of myocardial Cx43.

关键词： Exercise Preconditioning Exhaustive exercise Myocardial injury Cardioprotection Connexin 43