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SENP2-mediated SERCA2a deSUMOylation increases calcium overload in cardiomyocytes to aggravate myocardial ischemia/reperfusion injury

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Chinese Medical Journal 2023年第20期136卷 2496-2507页

作者： Yuanyuan Luo Shuaishuai Zhou Tao Xu Wanling Wu Pingping Shang Shuai Wang Defeng Pan Dongye Li Department of Cardiology The Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu 221006China Institute of Cardiovascular Disease Research Xuzhou Medical UniversityXuzhouJiangsu 221002China

Background:Sarcoplasmic reticulum calcium ATPase 2a(SERCA2a)is a key protein that maintains myocardial Ca2+*** present study aimed to investigate the mechanism underlying the SERCA2a-SUMOylation(small ubiquitinlike modifier)process after ischemia/reperfusion injury(I/RI)in vitro and in ***:calcium transient and systolic/diastolic function of cardiomyocytes isolated from Serca2a knockout(KO)and wildtype mice with I/RI were ***-relevant protein expression and localization were detected by quantitative real-time PCR(RT-qPCR),Western blotting,and immunofluorescence in vitro and in ***2a-SUMOylation,infarct size,and cardiac function of Senp1 or Senp2 overexpressed/suppressed adenovirus infected cardiomyocytes,were detected by immunoprecipitation,triphenyltetrazolium chloride(TTC)-Evans blue staining,and echocardiography ***:The results showed that the changes of Fura-2 fluorescence intensity and contraction amplitude of cardiomyocytes decreased in the I/RI groups and were further reduced in the Serca2a KO+I/RI ***1 and Senp2 messenger ribose nucleic acid(mRNA)and protein expression levels in vivo and in cardiomyocytes were highest at 6 h and declined at 12 h after I/***,the highest levels in HL-1 cells were recorded at 12 ***2 expression increased in the cytoplasm,unlike that of *** of Senp2 protein reversed the I/RI-induced Serca2a-SUMOylation decline,reduced the infarction area,and improved cardiac function,while inhibition of Senp1 protein could not restore the above ***:I/RI activated Senp1 and Senp2 protein expression,which promoted Serca2a-deSUMOylation,while inhibition of Senp2 expression reversed Serca2a-SUMOylation and improved cardiac function.

关键词： Myocardial ischemia Reperfusion injury Sarcoplasmic reticulum calcium-transporting ATPases Sentrin/SUMOspecific protease calcium overload

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18β-Glycyrrhetinic Acid Improves Cardiac Diastolic Function by Attenuating Intracellular calcium overload

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Current Medical Science 2020年第4期40卷 654-661页

作者： Jun HAN Guan-hua SU Yu-hui WANG Yong-xin LU Hong-liang ZHAO Xin-xin SHUAI Department of Cardiology Wuhan Fourth HospitalPuai HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430033China Department of Cardiology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China

Summary:Ranolazine,a late sodium current inhibitor,has been demonstrated to be effective on heart failure.18B-glycyrrhetinic acid(18β-GA)has the similar inhibitory effect on late sodium ***,its effect on diastolic function is still *** study aimed to determine whether 18β-GA can improve the diastolic function and to explore the underlying *** male Sprague Dawley(SD)rats of Langendorff model were randomly divided into the following groups:group A,normal cardiac perfusion group;group B,ischemia-reperfusion group;group C,ischemia-reperfusion with anemoniasulcata toxinⅡ(ATX-Ⅱ);group D,ranolazine group;and group E,18β-GA group with four different ***,a pressure-overloaded rat model induced by trans-aortic constriction(TAC)was *** and hemodynamics were used to evaluate diastolic function at 14th day after *** of free intracellular calcium(Ca27)concentration was indirectly detected by laser scanning confocal microscope to confirm the inhibition of late sodium *** the intervention of ATX-Ⅱon ischemia reperfusion injury group,5 umol/L ranolazine,and 5,10,20,40μmol/L 18β-GA could improve ATX-I-induced cardiac diastolic dysfunction.630 mg/kg glycyrrhizin tablets could improve cardiac diastolic function in the pressure-overloaded rats.18B-GA and ranolazine had similar effects on reducing the free calcium in *** study demonstrates that 18B-GA and glycyrrhizin could improve diastolic dysfunction induced by ischemia-reperfusion injury in Langendorff-perfused rat hearts and pressure-overloaded *** mechanism may be attributed to the inhibition of enhanced late sodium currents.

关键词： glycyrrhetinic acid diastolic function calcium overload

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Blocking Cyclic Adenosine Diphosphate Ribose-mediated calcium overload Attenuates Sepsis-induced Acute Lung Injury in Rats

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Chinese Medical Journal 2016年第14期129卷 1725-1730页

作者： Qian-Yi Peng Yu Zou Li-Na Zhang Mei-Lin Ai Wei Liu Yu-Hang Ai Department of Critical Care Medicine Xiangya Hospital Central South University Changsha Hunan 410008 China Department of Anesthesia Xiangya Hospital Central South University Changsha Hunan 410008 China

Background： Acute lung injury （ALI） is a common complication of sepsis that is associated with high mortality, lntracellular Ca^2＋ overload plays an important role in the pathophysiology of sepsis-induced ALl, and cyclic adenosine diphosphate ribose （cADPR） is an important regulator of intracellular Ca^2＋ mobilization. The cluster of differentiation 38 （CD38）/cADPR pathway has been found to play roles in multiple inflammatory processes but its role in sepsis-induced ALl is still unknown. This study aimed to investigate whether the CD38/cADPR signaling pathway is activated in sepsis-induced ALl and whether blocking cADPR-mediated calcium overload attenuates ALl. Methods： Septic rat models were established by cecal ligation and puncture （CLP）. Rats were divided into the sham group, the CLP group, and the CLP＋ 8-bromo-cyclic adenosine diphosphate ribose （8-Br-cADPR） group. Nicotinamide adenine dinucleotide （NAD＋）, cADPR, CD38, and intracellular Ca^2＋ levels in the lung tissues were measured at 6, 12, 24, and 48 h after CLP surgery. Lung histologic injury, tumor necrosis factor （TNF）-a, malondialdehyde （MDA） levels, and superoxide dismutase （SOD） activities were measured. Results： NAD＋, cADPR, CD38, and intracellular Ca-＋ levels in the lungs of septic rats increased significantly at 24 h after CLP surgery. Treatment with 8-Br-cADPR, a specific inhibitor of cADPR, significantly reduced intracellular Ca^2＋ levels （P = 0.007）, attenuated lung histological injury （P = 0.023）, reduced TNF-a and MDA levels （P 〈 0.001 and P = 0.002, respectively） and recovered SOD activity （P = 0.031） in the lungs of septic rats. Conclusions： The CD38/cADPR pathway is activated in the lungs of septic rats, and blocking cADPR-mediated calcium overload with 8-Br-cADPR protects against sepsis-induced ALl.

关键词： Acute Lung Injury calcium overload Cyclic Adenosine Diphosphate Ribose Sepsis

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Sodium tashinoneⅡA sulfonate improves tachycardia-induced electrical remodeling through attenuating intracellular calcium overload

Sodium tashinoneⅡA sulfonate improves tachycardia-induced e...

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中国生理学会第24届全国会员代表大会暨生理学学术大会

作者：欧贤红李妙龄王璐珍宾晓红刘瑞杨艳曾晓荣泸州医学院

Introduction:Atrial fibrillation（AF）is the most common sustained arrhythmia in *** is well known that calcium overload is an important foundation for onset and development of AF.,and attenuating intracellular calcium overload is thought to be related to the success treatments of *** tashinoneⅡA sulfonate（DS-201）,a water-soluble derivative of Tanshinone ⅡA,block L-type calcium channel similar to those of *** some previous reports suggested that DS-201 significantly affect the cardiovascular diseases which might be related to calcium channel and sodium channel blockade,however,its effect on AF and relationship with calcium overload have been ***:To determine the effects of DS-201 on electrical remodeling of canine and its ***:Mongol canines were used for preparation of animal models with AF through rapid pacing left atrial appendage,then the effect of DS-201 on AF was determined by frequency and duration of *** the contractile and calcium transient were determined using video-based motion edge-detection system（Ion Optix）simultaneously in remodeling rat atrial ***:It was showed that DS-201 significantly reduced both the frequency and duration of AF（P＜0.05,n=5）.The frequency of AF was reduced from7.2±1.31 to 3.12±1.05,and the duration of AF was lowered from 5.2±2.13 s to 0.89±1.23 ***-201（10,50 and 100 m M）decreased the extent of cell shortening and the calcium transient amplitude on remodeling cells in a concentration-dependentmanner ***:DS-201 improves tachycardia-induced electrical remodeling of canine,which might relate to attenuating intracellular calcium overload.

关键词： Sodium tashinoneⅡA sulfonate atrium remodeling calcium overload

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Targeting on calcium overload mediated brain aging and PD

Targeting on calcium overload mediated brain aging and PD

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中国神经科学学会第十二届全国学术会议

作者： Rong Cai Lei Liu Center of Stroke Beijing Institute for Brain Disorders Capital Medical University

Objective Brain aging associates with increasing intracellular calcium and decreasing brain energy. These two processes are likely correlated. For instance, calcium overload may trigger mitochondrial fragmentation which decreases its energy production. As a feedback, decreased energy output results in failure to maintain calcium gradients across the membrane and promotes calcium overload. Therefore, calcium overload and energy failure together may accelerate brain aging（accelerated aging hypothesis）. Our previous study demonstrated that Miro/Vimar complex served as a mediator of calcium overload and mitochondrial fragmentation. Miro is a small GTPase, well known for its function to regulate mitochondrial morphology and transportation. Vimar is the guanine nucleotide exchange factor of Miro that we identified in Drosophila. The mammalian homolog of Vimar is RAP1 GDS1. Methods To test the accelerated aging hypothesis, we generated transgenic flies to overload calcium and performed genetic manipulation on Miro/Vimar complex. In rodent Parkinson disease（PD） models, energy failure due to mitochondrial dysfunction has been well known to play a key pathophysiological role. Therefore, we select to target energy failure in PD to test the potential application of the hypothesis. To restore cellular energy, our previous study showed that terazosin（TZ） can activate glycolysis in vitro. Here, we tested whether TZ might act as a neuroprotective agent in rodent models of PD. Results 1) calcium overload in the transgenic flies（overexpressed a leaky cation channel） reduced their locomotion ability, but no lifespan reduction, indicating calcium overload may enhance dementia in flies. 2) TZ could promote aerobic glycolysis and energy recovery in mouse brain in vivo. TZ showed strong rescue effects against the MPTP induced PD models in mice and the 6-OHDA induced PD model in rats. Conclusion Accelerated aging hypothesis is supported by our current results, but more work is still needed

关键词： Mitochondrial dysfunction Parkinson’s disease Energy failure calcium overload Brain aging Terazosin Aerobic glycolysis Miro/Vimar Drosophila genetics

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Restoring cellular calcium homeostasis to rescue ER stress by 1,2-bis(2-aminophenoxy)ethane-N,N,N’,N’-tetraacetic acid acetoxymethyl ester-loaded lipid-mPLGA hybrid-nanoparticles for acute kidney injury therapy

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Chinese Chemical Letters 2024年第3期35卷 337-345页

作者： Jingwen Zhang Jiahui Yan Yanan Wang Hong Liu Xueping Sun Yuchao Gu Liangmin Yu Changcheng Li Jun Wu Zhiyu He Frontiers Science Center for Deep Ocean Multispheres and Earth System and Key Laboratory of Marine Chemistry Theory and TechnologyMinistry of EducationOcean University of ChinaQingdao 266100China College of Chemistry and Chemical Engineering Ocean University of ChinaQingdao 266100China School of Medicine and Pharmacy Ocean University of ChinaQingdao 266003China Sanya Oceanographic Institution Ocean University of ChinaQingdao 572024China Bioscience and Biomedical Engineering Thrust The Hong Kong University of Science and Technology(Guangzhou)NanshaGuangzhou 511400China Division of Life Science The Hong Kong University of Science and TechnologyHong Kong 999077China

Early pathogenesis of ischemia-reperfusion(I/R)-induced acute kidney injury(AKI)is dominated by intracellular calcium overload,which induces oxidative stress,intracellular energy metabolism disorder,inflammatory activation,and a series of pathologic cascaded reactions that are closely intertwined with self-amplifying and interactive feedback loops,ultimately resulting in cell damage and kidney ***,most nanomedicines originate from the perspective of antioxidant stress,which can only quench existing reactive oxide species(ROS)but cannot prevent the continuous production of ROS,resulting in insufficient *** a safe and promising drug,BAPTA-AM is hydrolyzed into BAPTA by intracellular esterase upon entering cells,which can rapidly chelate with overloaded Ca^(2+),restoring intracellular calcium homeostasis,thus inhibiting ROS regeneration at the ***,we designed a KTP-targeting peptide-modified yolk-shell structure of liposome–poly(ethylene glycol)methyl ether-block-poly(L-lactide-co-glycolic)(mPLGA)hybrid nanoparticles(calcium overload/ROS generation at its source,blocking the endoplasmic reticulum(ER)apoptosis pathway(ATF4–CHOP–Bax/Bcl-2,Casp-12–Casp-3)and the inflammatory pathway(TNF-α–NF-κB–IL-6 axes),thus alleviating pathological changes in kidney tissue,thereby inhibiting the expression of renal tubular marker kidney injury mole

关键词： BAPTA-AM calcium overload Acid-responsive AKI ER stress

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Biodegradable calcium sulfide-based nanomodulators for H_(2)S-boosted Ca^(2+)-involved synergistic cascade cancer therapy

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Acta Pharmaceutica Sinica B 2022年第12期12卷 4472-4485页

作者： Chuchu Lin Chenyi Huang Zhaoqing Shi Meitong Ou Shengjie Sun Mian Yu Ting Chen Yunfei Yi Xiaoyuan Ji Feng Lv Meiying Wu Lin Mei School of Pharmaceutical Sciences(Shenzhen) Shenzhen Campus of Sun Yat-sen UniversityShenzhen 518107China Tianjin Key Laboratory of Biomedical Materials Key Laboratory of Biomaterials and Nanotechnology for Cancer ImmunotherapyInstitute of Biomedical EngineeringChinese Academy of Medical Sciences and Peking Union Medical CollegeTianjin 300192China Academy of Medical Engineering and Translational Medicine Medical CollegeTianjin UniversityTianjin 300072China

Hydrogen sulfide(H_(2)S)is the most recently discovered gasotransmitter molecule that activates multiple intracellular signaling pathways and exerts concentration-dependent antitumor effect by interfering with mitochondrial respiration and inhibiting cellular ATP *** by the fact that H_(2)S can also serve as a promoter for intracellular Ca^(2+)influx,tumor-specific nanomodulators(I-CaS@PP)have been constructed by encapsulating calcium sulfide(CaS)and indocyanine green(ICG)into methoxy poly(ethylene glycol)-b-poly(lactide-co-glycolide)(PLGA-PEG).I-CaS@PP can achieve tumor-specific biodegradability with high biocompatibility and pH-responsive H_(2)S *** released H_(2)S can effectively suppress the catalase(CAT)activity and synergize with released Ca^(2+)to facilitate abnormal Ca^(2+)retention in cells,thus leading to mitochondria destruction and amplification of oxidative *** dysfunction further contributes to blocking ATP synthesis and downregulating heat shock proteins(HSPs)expression,which is beneficial to overcome the heat endurance of tumor cells and strengthen ICG-induced photothermal *** a H_(2)S-boosted Ca^(2+)-involved tumor-specific therapy exhibits highly effective tumor inhibition effect with almost complete elimination within 14-day treatment,indicating the great prospect of CaS-based nanomodulators as antitumor therapeutics.

关键词： calcium sulfide Hydrogen sulfide calcium overload Oxidative stress Photothermal therapy Biodegradability Controllable release Nanomodulators

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Liraglutide directly protects cardiomyocytes against reperfusion injury possibly via modulation of intracellular calcium homeostasis

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Journal of Geriatric Cardiology 2017年第1期14卷 57-66页

作者： Shun-Ying HU Ying ZHANG Ping-Jun ZHU Hao ZHOU Yun-Dai CHEN Department of Cardiology Chinese PLA General Hospital Beijing China

Background Liraglutide is glucagon-like peptide-1 receptor agonist for treating patients with type 2 diabetes mellitus. Our previous studies have demonstrated that liraglutide protects cardiac function through improving endothelial function in patients with acute myocardial infarction undergoing percutaneous coronary intervention. The present study will investigate whether liraglntide can perform direct protective effects on cardiomyocytes against reperfusion injury. Methods In vitro experiments were performed using H9C2 cells and neonatal rat ventricular cadiomyocytes undergoing simulative hypoxia/reoxygenation （H/R） induction. Cardiomyocytes apoptosis was detected by fluorescence TUNEL. Mitochondrial membrane potential （AWm） and intracellular reactive oxygen species （ROS） was assessed by JC-1 and DHE, respectively. Fura-2/AM was used to measure intracellular Ca2＋ concentration and calcium transient. Immtmofluorescence staining was used to assess the expression level of sarcoplasmic reticulum Ca2＋-ATPase （SERCA2a）. In vivo experiments, myocardial apoptosis and expression of SERCA2a were detected by colorimetric TUNEL and by immunofluorescence staining, respectively. Results In vitro liraglutide inhibited cardiomyotes apoptosis against H/R. △mψ of cardiomyocytes was higher in liraglntide group than H/R group. H/R increased ROS production in H9C2 cells which was attenuated by liraglutide. Liraglutide significantly lowered Ca2＋ overload and improved calcium transient compared with H/R group, lmmunofluorescence staining results showed liraglutide promoted SERCA2a expression which was decreased in H/R group. In ischemia/reperfusion rat hearts, apoptosis was significantly attenuated and SERCA2a expression was increased by liraglutide compared with H/R group. Conclusions Liraglutide can directly protect cardiomyocytes against reperfusion injury which is possibly through modulation of intracellular calcium homeostasis.

关键词： calcium overload Cardiomyocyte Liraglutide Reperfusion injury Sarcoplasmic reticulum Ca2+-ATPase

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Does closure of acid-sensing ion channels reduce ischemia/reperfusion injury in the rat brain?

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Neural Regeneration Research 2013年第13期8卷 1169-1179页

作者： Jie Wang Yinghui Xu Zhigang Lian Jian Zhang Tingzhun Zhu Mengkao Li Yi Wei Bin Dong Department of Neurosurgery the First Affiliated Hospital of Dalian Medical University

Acidosis is a common characteristic of brain damage. Because studies have shown that permeable Ca2＋-acid-sensing ion channels can mediate the toxic effects of calcium ions, they have become new targets against pain and various intracranial diseases. However, the mechanism associated with expression of these channels remains unclear. This study sought to observe the expression characteristics of permeable Ca2＋-acid-sensing ion channels during different reperfusion inflows in rats after cerebral ischemia. The rat models were randomly divided into three groups： adaptive ischemia/reperfusion group, one-time ischemia/reperfusion group, and severe cerebral ischemic injury group. Western blot assays and immunofluorescence staining results exhibited that when compared with the one-time ischemia/reperfusion group, acid-sensing ion channel 3 and Bcl-x/I expression decreased in the adaptive ischemia/reperfusion group. Calmodulin expression was lowest in the adaptive ischemia/reperfusion group. Following adaptive reperfusion, common carotid artery flow was close to normal, and the pH value improved. Results verified that adaptive reperfusion following cerebral ischemia can suppress acid-sensing ion channel 3 expression, significantly reduce Ca2＋ influx, inhibit calcium overload, and diminish Ca2＋ toxicity. The effects of adaptive ischemia/reperfusion on suppressing cell apoptosis and relieving brain damage were better than that of one-time ischemia/reperfusion.

关键词： neural regeneration brain injury acid-sensing ion channel 3 cerebral ischemia reperfusion apoptosis calmodulin calcium overload nerve cells grants-supported paper neuroregeneration

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P2X_7 receptors in cerebral ischemia

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Neuroscience Bulletin 2013年第3期29卷 390-398页

作者： Hui-Yu Bai Ai-Ping Li Department of Physiology Dalian Medical University

Cerebral ischemia is one of the most common diseases resulting in death and disability in aged people. It leads immediately to rapid energy failure, ATP depletion, and ionic imbalance, which increase extracellular ATP levels and accordingly activate P2X7 receptors. These receptors are ATP-gated cation channels and widely distributed in nerve cells, especially in the immunocompetent cells of the brain. Currently, interest in the roles of P2Xz receptors in ischemic brain injury is growing. In this review, we discuss recent research progress on the actions of P2X7 receptors, their possible mechanisms in cerebral ischemia, and the potential therapeutic value of P2X7 receptor antagonists which may provide a new target both for clinical and for research purposes.

关键词： P2X7 receptor cerebral ischemia neurotoxicity calcium overload neuroinflammation neurotrans-mitter receptor antagonist

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