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Quality Control System of the Endoplasmic Reticulum and Related Diseases

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Acta Biochimica et Biophysica Sinica 2006年第4期38卷 219-226页

作者： Jun-Chao WU Zhong-qin LIANG zheng-hong qin* Department of Pharmacology,School of Medicine,Soochow University,Suzhou 215123,China Department of Pharmacology School of Medicine Soochow UniversitySuzhou 215123 China

The quality control (QC) system of the endoplasmic reticulum (ER) is an important monitoringmechanism in the protein maturation process,which ensures export of properly folded proteins from the *** or incompletely folded proteins are retained in the ER for refolding or degradation by the ER-residing *** calnexin/calreticulin cycle and ER-associated degradation are the key elements *** two mechanisms work together to allow incorrectly folded proteins have additional opportunitiesto achieve their native *** QC dysfunction is involved in many diseases caused by mutantproteins,many of which are causes of neurodegenerative disorders.A better understanding of molecularregulation in the QC system will uncover the molecular pathogenic mechanisms of many diseases caused byprotein misfolding and help discover novel strategies for preventing or treating these diseases.

关键词： protein folding quality control calnexin/calreticulin cycle endoplasmic reticulum-associated degradation protein misfolding disease

Prostaglandin A1 inhibits increases in intracellular calcium concentration,TXA2 production and platelet activation

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Acta Pharmacologica Sinica 2006年第5期27卷 549-554页

作者： Yi ZHU Zhen-lun GU Zhong-qin LIANG Hui-lin ZHANG zheng-hong qin~2 Department of Pharmacology,Soochow University School of Medicine,Suzhou 215123,China Department of Pharmacology Soochow University School of Medicine Suzhou China

Aim:In our previous studies we found that cyclopentenane prostaglandin A1(PGA1) had neuroprotective effects in a rodent ischemic *** the presentstudy we aimed to investigate the inhibitory effect of PGA1 on platelet ***:The rate of aggregation of human platelets was measured by *** rate of adhesion of platelets to cultured endothelial cells wasdetermined by using [~3H]-adenine labeled platelets.5-Hydroxytryptamine releasefrom platelets was measured with O-phthaldialdehyde *** levels of TXB2,a stable metabolite of TXA2,were determined by *** in platelet morphology were observed using an electronmicroscope,and the intraplatelet free calcium concentrations were measured withFluo-3/AM FCM ***:PGA1 significantly inhibited thrombin-,col-lagen-and ADP-induced aggregation and adhesion of *** morphologi-cal changes of platelets induced by thrombin were blocked by ***1inhibited the release of 5-hydroxytyptamine from dense granules and the synthe-sis of ***:PGA1 inhibits the activation of platelets probablythrough blocking increases in intracellular calcium concentration and TXA2synthesis.

关键词： prostaglandin A1 platelet aggregation calcium TXA2

Molecular mechanism and regulation of autophagy

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Acta Pharmacologica Sinica 2005年第12期26卷 1421-1434页

作者： Ya-ping YANG~2 Zhong-qin LIANG~2 Zhen-lun GU~2 zheng-hong qin~(2,3) 2 Department of Pharmacology,Soochow University School of Medicine,Suzhou 215007,China Department of Pharmacology Soochow University School of Medicine Suzhou China

Autophagy is a major cellular pathway for the degradation of long-lived pro-teins and cytoplasmic organelles in eukaryotic cells.A large number of intracellu-lar/extracellular stimuli,including amino acid starvation and invasion ofmicroorganisms,are able to induce the autophagic response in *** discov-ery of the ATG genes in yeast has greatly advanced our understanding of themolecular mechanisms participating in autophagy and the genes involved in regu-lating the autophagic *** yeast genes have mammalian homologs,suggesting that the basic machinery for autophagy has been evolutionarily con-served along the eukaryotic *** regulation of autophagy is a very com-plex *** signaling pathways,including target of rapamycin(TOR)ormammalian target of rapamycin(mTOR),phosphatidylinositol 3-kinase-I(PI3K-I)/PKB,GTPases,calcium and protein synthesis all play important roles in *** molecular mechanisms and regulation of autophagy are dis-cussed in this review.

关键词： autophagy phosphatidylinositol 3-kinase Atg protein mTOR protein protein degradation

Neuronal autophagy in cerebral ischemia

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Neuroscience Bulletin 2012年第5期28卷 658-666页

作者： Feng Xu Jin-Hua Gu zheng-hong qin Department of Neurosurgery Huashan Hospital Fudan University Shanghai 200040 China Department of Pharmacology Nantong University School of Medicine Nantong 226001 China Department of Pharmacology and Laboratory of Aging and Nervous Diseases Soochow University School of Pharma-ceutical Science Suzhou 215123 China

Autophagy has evolved as a conserved process for the bulk degradation and recycling of cytosolic components, such as long-lived proteins and organelles. In neurons, autophagy is important for homeostasis and protein quality control and is maintained at relatively low levels under normal conditions, while it is upregulated in response to pathophysiological conditions, such as cerebral ischemic injury. However, the role of autophagy is more complex. It depends on age or brain maturity, region, severity of insult, and the stage of ischemia. Whether autophagy plays a beneficial or a detrimental role in cerebral ischemia depends on various pathological conditions. In this review, we elucidate the role of neuronal autophagy in cerebral ischemia.

关键词： autophagy cerebral ischemia neuron apoptosis necrosis

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Partially Loaded Cavity Analysis by Using the 2-D FDTD Method

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Chinese Physics Letters 2011年第11期28卷 257-260页

作者： YAO Bin zheng qin-hong PENG Jin-Hui Zhong Ru-Neng XIANG Tai XU Wan-Song College of Physical Science and Technology Yunnan UniversityKunming 650092 School of Physics and Electronic Information Yunnan Normal UniversityKunming 650092 Faculty of Materials and Metallurgical Engineering Kunming University of Science and TechnologyKunming 650093

A compact two-dimensional(2-D)finite-difference time-domain(FDTD)method is proposed to calculate the resonant frequencies and quality factors of a partially loaded cavity that is uniform in the𝑧-direction and has an arbitrary cross section in the𝑥x–y𝑦*** the description of𝑧dependence by𝑘z,the three-dimensional(3-D)problem can be transformed into a 2-D ***,less memory and CPU time are required as compared to the conventional 3-D FDTD *** representative examples,a half-loaded rectangular cavity,an inhomogeneous cylindrical cavity and a cubic cavity loaded with dielectric post,are presented to validate the utility and efficiency of the proposed method.

关键词： FDTD cavity loaded

Caspase-1 inhibitor Ac-YVAD-CHO attenuates quinolinic acid-induced increases in p53 and apoptosis in rat striatum

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Acta Pharmacologica Sinica 2005年第2期26卷 150-154页

作者： Yi CAO Zhen-lun GU Fang LIN Rong HAN zheng-hong qin Department of Pharmacology,Soochow University School of Medicine,Suzhou 215007,China Department of Pharmacology Soochow University School of Medicine Suzhou China

Aim:To study the effects of the caspase-1 inhibitor Ac-YVAD-CHO on quinolinicacid(QA)-induced ***:Rats were pre-treated with intrastriatalinfusion of Ac-YVAD-CHO(2-8μg)before intrastriatal injection of QA(60 nmol).Striatal total proteins,genomic DNA,and nuclear proteins were *** of Ac-YVAD-CHO on QA-induced caspase-1 activity,internucleosomalDNA fragmentation, IκB-α degradation,NF-κB,and AP-1 activation,and increasesin p53 protein levels were measured with enzyme assays,agarose gel electro-phoresis,electrophoresis mobility shift assays,and Western blot ***:Pre-treatment with Ac-YVAD-CHO inhibited QA-induced internucleo-somal DNA ***-YVAD-CHO inhibited QA-induced increases incaspase-1 activity and p53 protein levels,but had no effect on QA-induced IκB-αdegradation,NF-κB or AP-1 ***:Caspase-1 is involved inQA-induced p53 upregulation but not IκB-α *** of caspase-1attenuates QA-induced apoptosis in rat striatum.

关键词： caspase 1 Ac-YVAD-CHO Huntington disease protein p53 NF-kappaB inhibitor alpha apoptosis NF-kappaB

Animal models of Huntington's disease: implications in uncovering pathogenic mechanisms and developing therapies

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Acta Pharmacologica Sinica 2006年第10期27卷 1287-1302页

作者： Lin-hui WANG~2 zheng-hong qin~(3,4) Departments of ~2Physiology and ~3Pharmacology,Soochow University School of Medicine,Suzhou 215123,China Department of Physiology Soochow University School of Medicine Suzhou China Department of Pharmacology Soochow University School of Medicine Suzhou China

Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder,which is caused by an abnormal expansion of Cytosine Adenine Guanine (CAG)trinucleotide repeat in the gene making huntingtin (Htt).Despite intensiveresearch efforts devoted to investigate molecular mechanisms of pathogenesis,effective therapy for this devastating disease is still not available at *** of various animal models of HD has offered alternative approachesin the study of HD molecular *** HD models,including chemical-induced models and genetic models,mimic some aspects of HD symptoms *** date,however,there is no ideal model which replicates all of theessential features of neuropathology and progressive motor and cognitive impair-ments of human *** a result,our understanding of molecular mechanisms ofpathogenesis in HD is still limited.A new model is needed in order to uncover thepathogenesis and to develop novel therapies for *** this review we discussedusefulness and limitations of various animal and cellular models of HD in uncov-ering molecular mechanisms of pathogenesis and developing novel therapies forHD.

关键词： Huntington’s disease huntingtin neurodegeneration animal models

The role of DRAM1 in autophagy and cell survival

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The role of DRAM1 in autophagy and cell survival

TP53-induced glycolysis and apoptosis regulator alleviates hypoxia/ischemia-induced microglial pyroptosis and ischemic brain damage

中国神经科学学会第十二届全国学术会议

作者： zheng-hong qin Soochow University

The damage regulated autophagy and apoptosis modulator 1（DRAM1） plays a role in TP53-mediated autophagy and apoptosis. However, the mechanisms by which DRAM1 regulates autophagy and apoptosis have not been fully understood. In our recent studies, we found that DRAM1 can be upregulated through both TP53-dependent and independent mechanisms and its upregulation played a role in autophagy. DRAM1 activated autophagy initiation process via Akt-p70 S6 K-S6 pathway. DRAM1 enhanced autophagy degradation process via activation of lysosomes. Therefore, DRAM1 can increase autophagy flux. DRAM1 also regulated apoptosis through lysosomal cathepsin B and BID. These studies suggest that DRAM1 plays important roles in autophagy activity and cell survival.

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Neural Regeneration Research 2021年第6期16卷 1037-1043页

作者： Lan-Lan Tan Xiao-Lu Jiang Li-Xiao Xu Gen Li Chen-Xi Feng Xin Ding Bin Sun zheng-hong qin Zu-Bin Zhang Xing Feng Mei Li Department of Neonatology Children’s Hospital of Soochow UniversitySuzhouJiangsu ProvinceChina Department of Pediatrics Research Institute Children’s Hospital of Soochow UniversitySuzhouJiangsu ProvinceChina Jiangsu Key Laboratory of Neuropsychiatric Diseases Department of PharmacologyCollege of Pharmaceutical SciencesSoochow UniversitySuzhouJiangsu ProvinceChina

Our previous studies have demonstrated that TP53-induced glycolysis and apoptosis regulator(TIGAR)can protect neurons after cerebral ischemia/***,the role of TIGAR in neonatal hypoxic-ischemic brain damage(HIBD)remains *** the present study,7-day-old Sprague-Dawley rat models of HIBD were established by permanent occlusion of the left common carotid artery followed by 2-hour *** 6 days before induction of HIBD,a lentiviral vector containing short hairpin RNA of either TIGAR or gasdermin D(LV-sh_TIGAR or LV-sh_GSDMD)was injected into the left lateral ventricle and *** aggressively proliferating immortalized(HAPI)microglial cell models of in vitro HIBD were established by 2-hour oxygen/glucose deprivation followed by 24-hour *** days before in vitro HIBD induction,HAPI microglial cells were transfected with LV-sh_TIGAR or LV-sh_*** results showed that TIGAR expression was increased in the neonatal rat cortex after HIBD and in HAPI microglial cells after oxygen/glucose deprivation/*** TIGAR knockdown in rats markedly worsened pyroptosis and brain damage after hypoxia/ischemia in vivo and in *** of exogenous nicotinamide adenine dinucleotide phosphate(NADPH)increased the NADPH level and the glutathione/oxidized glutathione ratio and decreased reactive oxygen species levels in HAPI microglial cells after oxygen/glucose deprivation/***,exogenous NADPH blocked the effects of TIGAR knockdown in neonatal HIBD in vivo and in *** findings show that TIGAR can inhibit microglial pyroptosis and play a protective role in neonatal *** study was approved by the Animal Ethics Committee of Soochow University of China(approval No.2017LW003)in 2017.

关键词： hypoxic-ischemic brain damage in vitro in vivo microglia NADPH pyroptosis ROS TIGAR

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