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YBX1 inhibits mitochondrial-mediated apoptosis in ischemic heart through the PI3K/AKT signaling pathway

Frigid Zone Medicine 2024年第1期4卷 51-64页

作者： Fangfang Bi Miao Cao Yuquan Wang Qingming Pan Zehong Jing Danyang Bing Lifang Lyu Tong Yu Tianyu Li Xuelian Li Haihai Liang Hongli Shan Yuhong Zhou Department of pharmacology(State-province key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin 150081China Shanghai Frontiers Science Research Center for Druggability of Cardiovascular noncoding RNA Institute for Frontier Medical TechnologyShanghai University of Engineering ScienceShanghai 201620China Department of Basic Medicine Xiamen Medical CollegeXiamen 361023China

Background:Myocardial infarction(MI)is associated with higher morbidity and mortality in the world,especially in cold ***1 is an RNA-binding protein that is required for pathological growth of cardiomyocyte by regulating cell growth and protein *** YBX1,as an individual RNA-binding protein,regulates cardiomyocytes through signaling cascades during myocardial infarction remain largely ***:In vivo,the mouse MI model was induced by ligating the left anterior descending coronary artery(LAD),and randomly divided into sham operation group,MI group,MI+YBX1 knockdown/overexpression group and MI+negative control(NC)*** protective effect of YBX1 was verified by echocardiography and triphenyltetrazolium chloride *** vitro,mitochondrial-dependent apoptosis was investigated by using CCK8,TUNEL staining,reactive oxygen species(ROS)staining and JC-1 staining in hypoxic neonatal mouse cardiomyocytes(NMCMs).Results:YBX1 expression of cardiomyocytes was downregulated in a mouse model and a cellular model on the ischemic *** to mice induced by MI,YBX1 overexpression mediated by adeno-associated virus serotype 9(AAV9)vector reduced the infarcted size and improved cardiac *** of endogenous YBX1 by shRNA partially aggravated ischemia-induced cardiac *** hypoxic cardiomyocytes,YBX1 overexpression decreased lactic dehydrogenase(LDH)release,increased cell viability,and inhibited apoptosis by affecting the expression of apoptosis related proteins,while knockdown of endogenous YBX1 by siRNA had the opposite *** of YBX1 restored mitochondrial dysfunction in hypoxic NMCMs by increasing mitochondrial membrane potential and ATP content and decreasing *** hypoxic NMCMs,YBX1 overexpression increased the expression of phosphorylated phosphatidylinositol 3 kinase(PI3K)/AKT,and the anti-apoptosis effect of YBX1 was eliminated t by LY294002,PI3K/AKT ***:YBX1 protected the heart

关键词： YBX1 PI3K/AKT apoptosis mitochondrial function myocardial infarction

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Electroacupuncture Alleviates HIF1-α-mediated Early Mitophagy in Spinal Cord Injury

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Clinical Complementary Medicine and pharmacology 2024年第1期4卷 26-35页

作者： Rong Hu Xingying Wu Kelin He Mengting Shi Haipeng Xu Yi Chen Bowen Chen Lei Wu Ruijie Ma Kang Liang key laboratory of Acupuncture and Neurology of Zhejiang province The Third School of Clinical Medicine(School of Rehabilitation Medicine)Zhejiang Chinese Medical UniversityHangzhou 310053ZhejiangChina Department of Acupuncture and Moxibustion The Third Affiliated Hospital of Zhejiang Chinese Medical University(Zhongshan Hospital of Zhejiang Province)Zhejiang Chinese Medical UniversityHangzhou 310053ZhejiangChina

Background:The inhibitory microenvironment around spinal cord injury(SCI)severely restricted functional repair after *** was one of the important measures to maintain cellular homeostasis and ensure the harmonious nerve cell ***-inducible factor1α(HIF1-α)can mediate mitochondrial autophagy in neurodegenerative diseases,but the mechanisms are complex and diverse,which need to be further *** plays a significant role in improving the neural microenvironment after spinal cord injury,promote long-term neurological function recovery in SCI patients,but whether electroacupuncture can participate in HIF1-α mediated mitophagy remains ***:Investigated the effects of HIF1-α on mitochondrial autophagy in rats with spinal cord contusion and the potential mechanism of ***:Following the successful construction of an SCI model of Sprague-Dawley rat utilizing a modified Allen method,electroacupuncture intervention was performed at T9 and T11 Jiaji acupoint(EX-B2),with further molecular biology and morphology examined by *** observe the effect of HIF1-α on local damage repair,the stereotypic injection of Hif1a knockdown virus was performed,and the changes of mitophagy in damaged local area was detected employing Western blotting,real-time fluorescence quantitative PCR,immunofluorescence,transmission electron microscopy and Nissl ***:HIF1-α as well as its mitophagy receptor BNIP3 and NIX are upregulated after spinal cord ***-troacupuncture treatment or local inhibition of HIF1-α expression can reverse the early autophagy state after spinal cord injury,reduce cell apoptosis and injury area,promote neuronal ***:Electroacupuncture may serve as a promising strategy for spinal cord injury treatment,by alleviating HIF1-α mediated early mitochondrial autophagy.

关键词： Spinal cord injury Electroacupuncture Hypoxia-inducible factor1α Mitophagy

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Ethanol modulates sensory information processing in cerebellar cortex

Ethanol modulates sensory information processing in cerebell...

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中国神经科学学会第十二届全国学术会议

作者： Mao-Cheng Wu Guang-Jian Zhang De-Lai Qiu key laboratory of cellular function and pharmacology of jilin province Yanbian University

Overdose intake of ethanol can impair cerebellar cortical neurons to integrate and transfer external information, resulting in a dysfunction of cerebellar motor regulation or cerebellar ataxia. We recently investigated the effects of ethanol on sensory stimulation-evoked responses in the cerebellar cortex of urethane-anesthetized mice, by electrophysiological and pharmacological methods. We found that ethanol dosedependently inhibited the facial stimulation evoked field potential responses in cerebellar granule cell layer, whereas ethanol bidirectional modulate the sensory stimulation-evoked responses in molecular layer via GABAA receptor. In vivo patch-clamp recordings showed that ethanol dose-dependently inhibited the facial stimulation-evoked outward currents of cerebellar Purkinje cells（PCs）. The ethanol-induced inhibition of facial stimulation-evoked outward currents were significantly abrogated by cannabinoid receptor 1（CB1） antagonists and agonist. The ethanol-induced inhibition of facial stimulation-evoked outward currents was prevented by cerebellar surface perfusion of the PKA inhibitors H-89, but not by intracellular administration of the PKA inhibitor PKI. Our present results indicate that ethanol inhibits the facial stimulation-evoked outward currents by activating presynaptic CB1 receptors via the PKA signaling pathway, suggesting that ethanol overdose impairs sensory information processing, at least in part, by inhibiting GABA release from molecular layer interneurons onto PCs. In addition, ethanol inhibited the spontaneous CS-evoked pause in simple spike firing and in the amplitude of the afterhyperpolarization via activation of CB1 receptors in vivo in mice, suggesting that excessive ethanol intake inhibits climbing fiber–PC synaptic transmission by modulating CB1 receptors in the cerebellar cortex.

关键词： Ethanol Cerebellar Purkinje cell sensory stimulation in vivo whole-cell patch-clamp recording complex spike cannabinoids receptor 1 protein kinase A

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Mechanisms of facial stimulation evoked long-term synaptic plasticity in the cerebellar granule cell layer in vivo in mice

Mechanisms of facial stimulation evoked long-term synaptic p...

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中国神经科学学会第十二届全国学术会议

作者： Chang Ma Ke-Min Zhang Chun-Ping Chu De-Lai Qiu Yan-Hua Bing key laboratory of cellular function and pharmacology of jilin province Yan Bian University

Objective To study the properties and possible mechanisms of the long-term synaptic plasticity induced by the facial tactile stimulation at mossy fiber-granule cell（MF-GC） synapses in urethane-anesthetized mice, by field potential recording technique and pharmacological methods. Methods Adult ICR mice（6–8-week-old） were anesthetized with urethane, and tracheotomized to avoid respiratory obstruction. The craniotomy was drilled to expose the cerebellar surface corresponding to Crus II. Results Our results showed that 4 Hz facial stimulation evoked long-term depression（LTD） of MF-GC synaptic transmission. However, 20 Hz facial stimulation evoked long-term potentiation（LTP） at MF-GC synapses. The MF-GC LTP was prevented by N-methyl-Daspartic acid receptor（NMDA） receptor antagonist, and could be pharmacological induced by application of NMDA. Notably, blockade of protein kinase C（PKC） pathway, 20 Hz facial stimulation failed to induce the MF-GC LTP. In addition, the MF-GC LTP could be enhanced by blocking γ-aminobutyrate A（GABAA） and cannabinoids I（CB1） receptors activities, but was decreased by inhibiting of nitric oxide synthesis. These results indicated that high frequency facial stimulation induced an NMDA receptor dependent, GABAA receptor and NO involved, and PKC signaling required LTP of MFGC synaptic transmission in vivo in mice. Conclusion Our results suggest that the sensory stimulation evoked MF-GC synaptic plasticity might be involved in motor learning in living animals.

关键词： Cerebellar cortex Tactile stimulation Long-term synaptic plasticity Granule cell layer In vivo

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Recent development of hydrogen sulfide-releasing biomaterials as novel therapies:a narrative review

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Biomaterials Translational 2022年第4期3卷 250-263页

作者： Jingyu Fan Elizabeth Pung Yuan Lin Qian Wang Department of Chemistry and Biochemistry University of South CarolinaColumbiaSCUSA State key laboratory of Polymer Physics and Chemistry Changchun Institute of Applied ChemistryChinese Academy of SciencesChangchunJilin ProvinceChina

Hydrogen sulfide(H_(2)S)has been reported as an endogenous gasotransmitter that contributes to the modulation of a myriad of biological signalling pathways,which includes maintaining homeostasis in living organisms at physiological concentrations,controlling protein sulfhydration and persulfidation for signalling processes,mediating neurodegeneration,and regulating inflammation and innate immunity,*** a result,researchers are actively exploring effective approaches to evaluate the properties and the distribution of H_(2)S in ***,the regulation of the physiological conditions of H_(2)S in vivo introduces the opportunity to further study the molecular mechanisms by which H_(2)S regulates cellular *** recent years,many H_(2)S-releasing compounds and biomaterials that can deliver H_(2)S to various body systems have been developed to provide sustained and stable H_(2)S ***,various designs of these H_(2)S-releasing biomaterials have been proposed to aid in the normal conduction of physiological processes,such as cardioprotection and wound healing,by modulating different signalling pathways and cell *** biomaterials as a platform to control the delivery of H_(2)S introduces the opportunity to fine tune the physiological concentration of H_(2)S in vivo,a key to many therapeutic *** this review,we highlight recent research works concerning the development and application of H_(2)S-releasing biomaterials with a special emphasis to different release triggering conditions in in vivo *** believe that the further exploration of the molecular mechanisms underlying H_(2)S donors and their function when incorporated with various biomaterials will potentially help us understand the pathophysiological mechanisms of different diseases and assist the development of H_(2)S-based therapies.

关键词： biomaterials cardiovascular disease H_(2)S donors hydrogen sulfide wound healing

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Legionella pneumophila temporally regulates the activity of ADP/ATP translocases by reversible ADP-ribosylation

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mLife 2022年第1期1卷 51-65页

作者： Jiaqi Fu Pengwei Li Hongxin Guan Dan Huang Lei Song Songying Ouyang Zhao-Qing Luo Department of Biological Sciences Purdue Institute for InflammationImmunology and Infectious DiseasePurdue UniversityWest LafayetteIndianaUSA Provincial University key laboratory of cellular Stress Response and Metabolic Regulation The Key Laboratory of Innate Immune Biology of Fujian ProvinceBiomedical Research Center of South ChinaKey Laboratory of OptoElectronic Science and Technology for Medicine of the Ministry of EducationCollege of Life SciencesFujian Normal UniversityFuzhouChina key laboratory of Organ Regeneration and Transplantation of the Ministry of Education State Key Laboratory of Zoonotic DiseasesDepartment of Respiratory MedicineCenter for Pathogen Biology and Infectious DiseasesThe First Hospital of Jilin UniversityChangchunChina

The mitochondrion is an important signaling hub that governs diverse cellular functions,including metabolism,energy production,and *** the hundreds of effectors translocated into host cells by the Dot/Icm system of Legionella pneumophila,several are targeted to mitochondria but the function of most of them remains *** recent study found that the effector Ceg3 inhibits the activity of ADP/ATP translocases(ANTs)by ADP-ribosylation(ADPR).Here,we show that the effect of Ceg3 is antagonized by Larg1,an effector encoded by lpg0081,a gene that is situated next to ***1 functions to reverse Ceg3-mediated ADPR of ANTs by cleaving the N-glycosidic bond between the ADPR moiety and the modified arginine residues in ANTs,leading to restoration of their activity in ADP/ATP *** analysis of Larg1 and its complex with ADPR reveals that this ADPR glycohydrolase harbors a unique macrodomain that catalyzes the removal of ADPR modification on *** results also demonstrate that together with Ceg3,Larg1 imposes temporal regulation of the activity of ANTs by reversible ADPR during *** infection.

关键词： energy metabolism metaeffector mitochondria type IV secretion

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Group 3 innate lymphoid cells: intestinal patrolling guardians bullied by T cells

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cellular & Molecular Immunology 2023年第2期20卷 115-116页

作者： Xinping Lv Shan Zhu Jing Wu Jingtao Chen Cancer Center First Hospital of Jilin UniversityChangchun130021JilinChina laboratory for Tumor Immunology First Hospital of Jilin UniversityChangchun130061JilinChina

Since the discovery of group 3 innate lymphoid cells(ILC3s),many studies have reported that,in addition to T cells,ILC3s also play an indispensable role in intestinal immune surveillance,host defense,and homeostasis[1].Although both ILC3s and T cells regulate intestinal inflammation through the secretion of interleukin(IL)-22,differences in the behaviors of these two cell types,especially the dynamic shift and mechanism of ILC3 regulation between normal and inflammatory states,remain unclear.A recent paper by Jarade et al.[2]published in Nature Immunology reported that intestinal ILC3s under basal conditions are immotile and arrested in the presence of T ***,the environmental T cells,the microbiota,and the chemokine CCL25 jointly shape ILC3 patrolling behavior and their effector function of maintaining intestinal barrier integrity via *** findings facilitate the study of ILC biodynamics and ILC immune regulation and the search for therapeutic strategies for gastrointestinal diseases.

关键词： lymphoid jointly guard

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In vivo recognition of bioactive substances of Polygonum multiflorum for protecting mitochondria against metabolic dysfunction-associated fatty liver disease

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World Journal of Gastroenterology 2023年第1期29卷 171-189页

作者： Li-Ping Yu Yan-Juan Li Tao Wang Yu-Xuan Tao Mei Zhang Wen Gu Jie Yu Xing-Xin Yang College of Pharmaceutical Science Yunnan University of Chinese MedicineKunming 650500Yunnan ProvinceChina College of Pharmaceutical Science Yunnan Key Laboratory of Southern Medicine UtilizationKunming 650500Yunnan ProvinceChina

BACKGROUND Metabolic dysfunction-associated fatty liver disease(MAFLD)is a severe threat to human *** multiflorum(PM)has been proven to remedy mitochondria and relieve MAFLD,but the main pharmacodynamic ingredients for mitigating MAFLD remain *** To research the active ingredients of PM adjusting mitochondria to relieve highfat diet(HFD)-induced MAFLD in *** Fat emulsion-induced L02 adipocyte model and HFD-induced MAFLD rat model were used to investigate the anti-MAFLD ability of PM and explore their action *** adipocyte model was also applied to evaluate the activities of PM-derived constituents in liver mitochondria from HFD-fed rats(mitochondrial pharmacology).PM-derived constituents in liver mitochondria were confirmed by ultra-high-performance liquid chromatography/mass spectrometry(mitochondrial pharmacochemistry).The abilities of PM-derived monomer and monomer groups were evaluated by the adipocyte model and MAFLD mouse model,*** PM repaired mitochondrial ultrastructure and prevented oxidative stress and energy production disorder of liver mitochondria to mitigate fat emulsion-induced cellular steatosis and HFD-induced ***-derived constituents that entered the liver mitochondria inhibited oxidative stress damage and improved energy production against cellular *** chemicals were found in the liver mitochondria of PM-administrated *** anti-steatosis ability of one monomer and the anti-MAFLD activity of the monomer group were *** PM restored mitochondrial structure and function and alleviated MAFLD,which may be associated with the remedy of oxidative stress and energy *** identified eight chemicals may be the main bioactive ingredients in PM that adjusted mitochondria to prevent ***,PM provides a new approach to prevent MAFLD-related mitochondrial *** pharmacology and pharmacochemistry further showed efficient strategies for de

关键词： Fatty liver Mitochondria Pharmacodynamic ingredients Polygonum multiflorum

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Roles of N-methyl-D-aspartate receptors during the sensory stimulation-evoked field potential responses in mouse cerebellar cortical molecular layer

Roles of N-methyl-D-aspartate receptors during the sensory s...

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中国生理学会张锡钧基金会第十四届全国青年优秀生理学学术论文交流及评奖会议、中国生理学会第十二届全国青年生理学工作者学术会议

作者：玄芳玲 Guang-Jian Zhang Yin-Hua Xu Chun-Ping Chu De-Lai Qiu key laboratory of cellular function and pharmacology of jilin province Yanbian University Department of Physiology and Pathophysiology College of MedicineYanbian University

The functions of N-methyl-D-aspartate receptors(NMDARs)in cerebellar cortex have been widely studied under in vitro condition,but their roles during the sensory stimulation-evoked responses in the

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Dihydroergotamine ameliorates liver fibrosis by targeting transforming growth factor β type Ⅱ receptor

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World Journal of Gastroenterology 2023年第20期29卷 3103-3118页

作者： Ke-Xin Zheng Shou-Li Yuan Meng Dong Han-Lin Zhang Xiao-Xiao Jiang Chun-Long Yan Rong-Cai Ye Hui-Qiao Zhou Li Chen Rui Jiang Zi-Yu Cheng Zhi Zhang Qi Wang Wan-Zhu Jin Wen Xie Center of Liver Diseases Beijing Ditan HospitalCapital Medical UniversityBeijing 100015China key laboratory of Animal Ecology and Conservation Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China Graduate School University of the Chinese Academy of SciencesBeijing 100049China Graduate School Agriculture College of Yanbian UniversityYanji 133002Jilin ProvinceChina

BACKGROUND The transforming growth factor β(TGFβ) signaling pathway plays a crucial role in the development of liver fibrosis by activating TGFβ type Ⅱ receptor(TGFβR2), followed by the recruitment of TGFβR1 finally triggering downstream signaling *** To find drugs targeting TGFβR2 that inhibit TGFβR1/TGFβR2 complex formation, theoretically inhibit TGFβ signaling pathway, and thereby ameliorate liver *** Food and Drug Administration-approved drugs were screened for binding affinity with TGFβR2 by virtual molecular docking. We identified 6 candidates and further explored their potential by Cell Counting Kit-8(CCK-8) cell cytotoxic experiment to validate toxicity and titrated the best cellular working concentrations. Next, we further demonstrated the detailed molecular working mechanisms using mutagenesis analysis. Finally, we used a mouse model to investigate its potential anti-liver fibrosis *** We identified 6 drug candidates. Among these 6 drugs, dihydroergotamine(DHE) shows great ability in reducing fibrotic gene expressions such as collagen, p-SMAD3, and α-SMA in TGFβ induced cellular model of liver fibrosis in LX-2 cells. Furthermore, we demonstrated that DHE binds to TGFβR2. Moreover, mutation of Leu27, Phe30, Thr51, Ser52, Ile53, and Glu55 of TGFβR2 disrupted the binding of TGFβR2 with DHE. In addition, DHE significantly improved liver fibrosis, as evidenced by Masson’s trichrome staining of liver sections. This is further supported by the width and the velocity of the portal vein, and serum markers of liver function. In line with those observations, DHE also decreased macrophages infiltration and extracellular matrix deposition in the *** DHE alleviates liver fibrosis by binding to TGFβR2 thereby suppressing TGFβ signaling pathway. We show here that as far as drug repurposing, DHE has great potential to treat liver fibrosis.

关键词： Liver fibrosis Transforming growth factorβ(TGFβ)signaling pathway TGFβtype II receptor(TGFβR2) Virtual screening Drug-repurposing Dihydroergotamine

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