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Arsenic trioxide induces multiple myeloma cell apoptosis via disruption of mitochondrial transmembrane potentials and activation of caspase-3

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Chinese Medical Journal 2001年第1期114卷 19-24页

作者：贾培敏陈国强黄晓君蔡循杨洁王龙周宇红沈玉雷周励余韵陈赛娟张学光王振义 Shanghai Institute of Hematology Ruijin Hospital Shanghai Second Medical University Shanghai 200025 China

OBJECTIVE: To investigate the response of multiple myeloma (MM) cells to arsenic trioxide (As2O3) and their possible mechanisms. METHODS: Two MM-derived cell lines RPMI8226 and U266 cells were used as in vitro models. Cell apoptosis was assessed by morphology, flow cytometry, and DNA gel electrophoresis. Mitochondrial transmembrane potentials (delta psi m) were evaluated by measuring cellular Rhodamine 123 staining intensity. Protein expression was analyzed using Western blot. RESULTS: Zero point one to 0.5 mumol/L As2O3 inhibited cell proliferation and 2.0 mumol/L As2O3 induced cell apoptosis, while 1.0 mumol/L As2O3 inhibited proliferation with a weak degree of apoptosis induction in RPMI8226 and U266 cell lines. As2O3-induced apoptosis was accompanied by mitochondrial transmembrane potentials (delta psi m) collapse and caspase-3 activation in the presence of intact membrane. Glutathione depleter buthionine sulfoximine enhanced, while disulfide bond-reducing agent dithiothreitol partially antagonized As2O3-induced delta psi m collapse and apoptosis in MM cells. All-trans retinoic acid (ATRA) could also induce apoptosis in RPMI8226 cells, but it did not show any cooperative effects with As2O3. CONCLUSION: As2O3 exerts apoptosis-inducing and growth-inhibiting effects on MM cells, and mitochondrium is a pivotal and common target of As2O3 for apoptosis induction.

关键词： Antineoplastic Agents Apoptosis Arsenicals Buthionine Sulfoximine Caspases Dose-Response Relationship, Drug Enzyme Activation Humans membrane potentials Mitochondria Multiple Myeloma Oxides Research Support, Non-U.S. Gov't Tretinoin Tumor Cells, Cultured

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JTE-522-induced apoptosis in human gastric adenocarinoma cell line AGS cells by caspase activation accompanying cytochrome C release,membrane translocation of Bax and loss of mitochondrial membrane potential

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World Journal of Gastroenterology 2002年第2期8卷 217-223页

作者： Hong-Liang Li Xiao-Hong Li Jun-Hua Lü Xian-Da Ren,Department of Pharmacology,Jinan University Pharmacy College,Guangzhou 510632,Guangdong Province,China Dan-Dan Chen,Department of Cardiology,First Affiliated Hospital,Zhongshan University,Guangzhou 510089,Guangdong Province,China Hai-Wei Zhang,Department of Pathology,Jinan University Medical College,Guangzhou 510632,Guangdong Province,China Cun-Chuan Wang,Department of laparoscopic surgery,First Affiliated Hospital,Jinan University Medical College,Guangzhou 510632,Guangdong Province,China Department of Pharmacology Jinan University Pharmacy College Guangzhou 510632 Guangdong Province China. tsam@***

AIM: To investigate the role of the mitochondrial pathway in JTE-522-induced apoptosis and to investigate the relationship between cytochrome C release, caspase activity and loss of mitochondrial membrane potential (Deltapsim). METHODS: Cell culture, cell counting, ELISA assay, TUNEL, flow cytometry, Western blot and fluorometric assay were employed to investigate the effect of JTE-522 on cell proliferation and apoptosis in AGS cells and related molecular mechanism. RESULTS: JTE-522 inhibited the growth of AGS cells and induced the apoptosis. Caspases 8 and 9 were activated during apoptosis as judged by the appearance of cleavage products from procaspase and the caspase activities to cleave specific fluorogenic substrates. To elucidate whether the activation of caspases 8 and 9 was required for the apoptosis induction, we examined the effect of caspase-specific inhibitors on apoptosis. The results showed that caspase inhibitors significantly inhibited the apoptosis induced by JTE-522. In addition, the membrane translocation of Bax and cytosolic release of cytochrome C accompanying with the decrease of the uptake of Rhodamin 123, were detected at an early stage of apoptosis. Furthermore, Bax translocation, cytochrome C release, and caspase 9 activation were blocked by *** and Z-IETD-CHO. CONCLUSION: The present data indicate a crucial association between activation of caspases 8, 9, cytochrome C release, membrane translocation of Bax, loss of Deltapsim and JTE-522-induced apoptosis in AGS cells.

关键词： Adenocarcinoma Stomach Neoplasms Amino Acid Chloromethyl Ketones Anti-Inflammatory Agents, Non-Steroidal Apoptosis Benzenesulfonates Caspases inhibitors Cyclooxygenase Inhibitors Cysteine Proteinase Inhibitors Cytochrome c Group Enzyme Activation Humans In Situ Nick-End Labeling membrane potentials Mitochondria Oxazoles Proto-Oncogene Proteins Proto-Oncogene Proteins c-bcl-2 Research Support, Non-U.S. Gov't Tumor Cells, Cultured bcl-2-Associated X Protein

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The role of membrane potential and calcium kinetic changes in the pathogenesis of vascular hyporeactivity during severe shock

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Chinese Medical Journal 2000年第1期113卷 59-64页

作者：赵克森刘杰金春华 China 510515

OBJECTIVE: To determine the role of membrane potential and intracellular calcium kinetic changes in producing vascular hyporeactivity during severe hemorrhagic shock. METHODS: Rats were subjected to hemorrhagic shock (HS) for 2 hours. The spinotrapezius muscle was prepared for microscopy and the responses of arterioles in the muscle to norepinephrine (NE) were tested. The resting membrane potentials of isolated arterial strips were measured with a microelectrode. membrane potential and intracellular Ca2+ ([Ca2+]i) changes in isolated arteriolar smooth muscle cells (ASMCs) were determined with fluorescent probes and a confocal microscopy. RESULTS: The arteriolar resting membrane potential was decreased from -36.7 +/- 6.3 mV in control to -29.2 +/- 5.3 mV concurrent with the increase of vasoreactivity to NE at 20 minutes after HS. At 120 minutes post-HS, the resting potential hyperpolarized to -51.9 +/- 9.1 mV, and NE stimulated [Ca2+]i increase was reduced to 50% of the control values during the appearance of arteriolar hyporeactivity, i.e. the NE threshold of the arteriolar response increased 15 fold 2 hours after the onset of hemorrhage as compared with normal animals. The state of vasoreactivity was closely related to the resting potential of vascular smooth muscle in hemorrhagic shock, with a correlation coefficient of 0.96. Treatment with glybenclamide, a selective blocker of ATP-sensitive K+ (KATP) channels, decreased the resting potential, increased NE-stimulated [Ca2+]i increase, and partially restored vasoreactivity in severe hemorrhagic shock. CONCLUSION: The results suggested that membrane hyperpolarization and the reduction of NE-stimulated [Ca2+]i increase in smooth muscle cells appeared to contribute to the vascular hyporeactivity in hemorrhagic shock. The mechanism is likely to involve in KATP channels.

关键词： Animals Calcium Glyburide membrane potentials Muscle, Smooth, Vascular Norepinephrine Potassium Channels Rats Rats, Sprague-Dawley Shock, Hemorrhagic

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Protective effects of Ginkgo biloba extract 761 against glutamate-induced neurotoxicity in cultured retinal neuron

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Chinese Medical Journal 2005年第11期118卷 948-952页

作者： WANGYun-song XULiang MAKe WANGShuang WANGJin-jin BeijingInstituteofOphthalmology TongrenEyeCenterBeijingTongrenHospitalCapitalUniversityofMedieialSeieneeBeiing100005China

A large part of neuronal death is the result of episodes of anoxia and ischaemia in the retina and other eye diseases, such as anterior ischemic optic neuropathy, glaucoma. The neuronal death is due to the accumulation of glutamate in the extracellular space. Glutamate is the primary excitatory neurotransmitter in the retina. However, excessive overactivation of glutamate receptors leads to excitotoxic neuronal cell death. Glutamate induces cell death by increasing the levels of intracellular Ca2+ in neurons, thereby leading to generation of free radicals and activation proteases, as well as transcriptional activation of specific cell death programs. Glutamate excitoxicity can also cause neuronal mitochondrial membrane potential (MMP) loss, which is associated with changes in mitochondrial function leading to a neuronal dysfunction.

关键词： retina neurons Ginkgo biloba extract 761 mitochondria membrane potentials

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Hyperpolarization caused by serotonin contributes to endothelium-dependent relaxations in the porcine coronary artery

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中国药理学报 1999年第12期20卷 1093-1096页

作者： Seung-Jung PARK Mikio NAKASHIMA Tetsuhiko NAGAO Paul M VANHOUTTE Center for Experimental Therapeutics Department of MedicineBaylor College of MedicineOne Baylor PlazaHoustonTX 77030USA

AIM:The present study was designed to investigate the contribution of membrane hyperpolarization to endothelium-dependent relaxations induced by serotonin in the porcine coronary ***:Rings with and without endothelium of porcine coronary arteries were suspended in conventional organ chambers for the measurement of isometric *** cell membrane potential of the vascular smooth muscle cells was measured using glass microelectrodes,in the presence of indometacin,ketanserin,and/or N^(ω)-***:Serotonin induced a transient endothelium-,and concentration-dependent relaxation in rings contracted with prostaglandin F_(2α)in the presence of N^(ω)-nitro-L-arginine(maximal relaxation;19%).The N^(ω)-nitro-L-arginine resistant relaxation was abolished by high K^(+)and tetrabutylammonium *** also caused an endothelium-,concentration-dependent membrane hyperpolarizations with a maximal amplitude *** nitro-L-arginine resistant relaxations and hyperpolarizations were abolished by methiothepin,but not by *** time course of the endothelium-dependent relaxations and hyperpolarizations was ***:These results suggest a contribution of cell membrane hyperpolarization to theendothelium-dependent relaxations induced by serotonin in the porcine coronary artery.

关键词： indomethacin ketanserin membrane potentials methiothepin nitric oxide potassium channels serotonin vascular endothelium

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Ethanol induced mitochondria injury and permeability transition pore opening: Role of mitochondria in alcoholic liver disease

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World Journal of Gastroenterology 2007年第16期13卷 2352-2356页

作者： Ming Yan Ping Zhu Hui-Min Liu Hai-Tao Zhang Li Liu Department of Digestive Diseases Qilu Hospital Shandong University Jinan 250012 Shandong Province China Jinan Infectious Disease Hospital Jinan 250012 ShandongProvince China

AIM: To observe changes of mitochondria and investigate the effect of ethanol on mitochondrial perme- ability transition pore (PTP), mitochondrial membrane potential (MMP, ΔΨm) and intracellular calcium concentration in hepatocytes by establishing an animal model of alcoholic liver disease (ALD). METHODS: Fourty adult male Wistar rats were randomly divided into two groups, the model group (20) was administered alcohol intragastrically plus an Oliver oil diet to establish an ALD model, and the control group (20) was given an equal amount of normal saline. The ultramicrostructural changes of mitochondria were observed under electron microscopy. Mitochondria of liver was extracted, and patency of PTP, mitochondrial membrane potential (ΔΨm), mitochondrial mass and intracellular calcium concentration of isolated hepacytes were detected by flow cytometry using rhodamine123 (Rh123), Nonyl-Acridine Orange and calcium fluorescent probe Fluo-3/AM, respectively. RESULTS: membrane and cristae were broken or disappeared in mitochondria in different shapes under electron microscopy. Some mitochondria showed U shape or megamitochondrion. In the model group, liver mitochondria PTP was broken, and mitochondria swelled, the absorbance at 450 nm, A540 decreased (0.0136 ± 0.0025 vs 0.0321 ± 0.0013, model vs control, P membrane potential (239.4638 ± 12.7263 vs 377.5850 ± 16.8119, P membrane potential and injury, and elevated intracellular Ca2+ production. Ethanol-induced chondriosome injury may be an important mechanism of alcoholic diseases.

关键词： Alcoholic liver disease Chondriosome Apoptosis Ultra microstructure membrane potentials Permeability transition pore Transmembrane potential chondriosome mass Ca^2+

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The development and applications of hybrid voltage indicators

The development and applications of hybrid voltage indicator...

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第十一届全国化学生物学学术会议

作者： Junqi Yang Peng Zou College of Chemistry and Molecular Engineering Peking University

Electrical signaling is the language among neurons for communications. The dynamics of membrane potentials is the basis of electrical propagation. We developed hybrid voltage indicators combined the better optical property from organic fluorogenic dyes and cellular specificity from genetically encoded voltage-sensing proteins for the new vistas in neuroscience researches, that we could non-invasively detect membrane potential changes in high temporal-spatial resolution and high throughput. In our work, we chose the reported non-pumping mutant, Ace2 N[1] from Acetabularia Rhodopsin II（Ace） as our voltage sensor and two kinds of self-labeling tags, HaloTag[2] and SNAP-tag[3] as the "ties" connected the organic fluorogenic ligands and Ace. The voltage-induced changes in the absorption spectrum of Ace2 N（eFRET[4] quencher） trigger strong voltage-dependent fluorescent changes of the ligated fluorescent ligands. We have tested expression, trafficking and capability of indicating membrane potential changes of hybrid indicators in HEK293 T cells and neurons. One mutant we designed for HaloTag related Volton[5] based indicators has improved ～50% sensitivity on indicating membrane potential changes compared to wild type. In the future, we will further do optimization for hybrid indicators and study the electrophysiology of body wall muscles of *** under the specific locomotion behaviors. We also expect to apply our indicators to test electrical signaling in other model animals, such as mouse, Drosophila and zebrafish.

关键词： membrane potentials hybrid voltage indicators C.elegans body wall muscles

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