1.Sixty years after Hsiang-Tung Chang's presentation on dendrite at the Cold Spring Harbor Symposium.
Acta Physiologica Sinica 2012;64(5):499-503
Sixty years elapsed since Chang (Hsiang-Tung Chang, Xiang-Tong Zhang) presented his seminal report "Cortical neurons with particular reference to the apical dendrite" at the Cold Spring Harbor Symposium. Thanks to the development of elaborated techniques through the 6 decades, our understanding of the dendrite has been pushed forward greatly: the backward and forward conductions during excitation, sodium and calcium conductances, chemical excitation by uncaging glutamate at a dimension of micrometer, and the quantitative study of chemical organization of postsynaptic density (PSD), etc. Though the progression is great, there are still tough problems in dendritic research, especially the integration through dendritic spine.
Calcium Signaling
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Dendrites
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physiology
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Glutamic Acid
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metabolism
2.The functional organisation of calcium signalling in exocrine acinar cells.
Journal of Korean Medical Science 2000;15(Suppl):S44-S45
No abstract available.
Animal
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Calcium Signaling/physiology*
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Exocytosis/physiology
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Pancreas/physiology*
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Pancreas/cytology
3.Calcium Signaling of Lysophosphatidylethanolamine through LPA1 in Human SH-SY5Y Neuroblastoma Cells.
Jung Min LEE ; Soo Jin PARK ; Dong Soon IM
Biomolecules & Therapeutics 2017;25(2):194-201
Lysophosphatidylethanolamine (LPE), a lyso-type metabolite of phosphatidylethanolamine, has been reported to be an intercellular signaling molecule. LPE mobilizes intracellular Ca²⁺ through G-protein-coupled receptor (GPCR) in some cells types. However, GPCRs for lysophosphatidic acid (LPA) were not implicated in the LPE-mediated activities in LPA GPCR overexpression systems or in SK-OV3 ovarian cancer cells. In the present study, in human SH-SY5Y neuroblastoma cells, experiments with LPA₁ antagonists showed LPE induced intracellular Ca²⁺ increases in an LPA₁ GPCR-dependent manner. Furthermore, LPE increased intracellular Ca²⁺ through pertussis-sensitive G proteins, edelfosine-sensitive-phospholipase C, 2-APB-sensitive IP₃ receptors, Ca²⁺ release from intracellular Ca²⁺ stores, and subsequent Ca²⁺ influx across plasma membranes, and LPA acted on LPA₁ and LPA₂ receptors to induce Ca²⁺ response in a 2-APB-sensitive and insensitive manner. These findings suggest novel involvements for LPE and LPA in calcium signaling in human SH-SY5Y neuroblastoma cells.
Calcium Signaling*
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Calcium*
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Cell Membrane
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GTP-Binding Proteins
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Humans*
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Neuroblastoma*
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Ovarian Neoplasms
4.Inhibition of Store-Operated Calcium Entry Protects Endothelial Progenitor Cells from H₂O₂-Induced Apoptosis.
Yan Wei WANG ; Ji Hang ZHANG ; Yang YU ; Jie YU ; Lan HUANG
Biomolecules & Therapeutics 2016;24(4):371-379
Store-operated calcium entry (SOCE), a major mode of extracellular calcium entry, plays roles in a variety of cell activities. Accumulating evidence indicates that the intracellular calcium ion concentration and calcium signaling are critical for the responses induced by oxidative stress. The present study was designed to investigate the potential effect of SOCE inhibition on H₂O₂-induced apoptosis in endothelial progenitor cells (EPCs), which are the predominant cells involved in endothelial repair. The results showed that H₂O₂-induced EPC apoptosis was reversed by SOCE inhibition induced either using the SOCE antagonist ML-9 or via silencing of stromal interaction molecule 1 (STIM1), a component of SOCE. Furthermore, SOCE inhibition repressed the increases in intracellular reactive oxygen species (ROS) levels and endoplasmic reticulum (ER) stress and ameliorated the mitochondrial dysfunction caused by H₂O₂. Our findings provide evidence that SOCE inhibition exerts a protective effect on EPCs in response to oxidative stress induced by H₂O₂ and may serve as a potential therapeutic strategy against vascular endothelial injury.
Apoptosis*
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Calcium Signaling
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Calcium*
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Endoplasmic Reticulum
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Endothelial Progenitor Cells*
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Oxidative Stress
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Reactive Oxygen Species
5.Laser scanning confocal microscopic imaging for Ca2 + oscillations of pancreatic acinar cells in mice.
Jing-Ke WANG ; Meng-Qin ZHAO ; Na-Na SUN ; Fang-Fan SUN ; Jie WU ; Jian-Xin SHEN ; Hai-Yan WANG
Chinese Journal of Applied Physiology 2014;30(4):373-377
OBJECTIVETo establish a simple but effective method of laser scanning confocal microscopic imaging for Ca2+ oscillations of pancreatic acinar cells in adult mice.
METHODSPancreatic acinar cells from adult Kunming mice were isolated acutely with collagenase, and then loaded with fluo-4-AM, a Ca2+ indicator. A laser scanning confocal microscope armed with 488 nm laser was employed to record the dynamic fluorescent signals in-time and synchronously while acetylcholine (ACh) was added in the pancreatic acinar cells.
RESULTS(1) The classic pancreatic acinar cell Ca2+ oscillations were induced by a certain concentration of ACh (100 nmol/L) successfully and steadily, which could be blocked by atropine completely. (2) Plasmic Ca2+ oscillations from different parts of one acinar cell were usually with different amplitudes and almost the same frequencies. But both of amplitudes and frequencies were different among different cells. (3) The acinar cell Ca2+ oscillations were induced by ACh in a concentration-dependent manner.
CONCLUSIONThe laser scanning confocal microscopic imaging for adult mouse pancreatic acinar cell Ca2+ oscillations was established successfully. The features of being easy to use, direct to see lively, high efficiency and good flexibility make it a popular tool for researchers to choose.
Acinar Cells ; chemistry ; Animals ; Calcium ; analysis ; Calcium Signaling ; Cells, Cultured ; Mice ; Microscopy, Confocal ; methods ; Pancreas ; cytology
6.Transient receptor potential ion channels and prostatic diseases.
Song FAN ; Chao-zhao LIANG ; Xian-sheng ZHANG
National Journal of Andrology 2007;13(3):242-245
Transient receptor potential (TRP) ion channels are widely distributed in different kinds of cells. TRP expresses highly in the prostatic cancer epithelia at different levels, but whether it expresses in chronic prostatitis epithelia or not remains poorly understood. Investigating the roles of TRP ion channels in the pathogenesis of prostatic diseases could afford us a new approach to their diagnosis and therapy.
Calcium Channels
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Calcium Signaling
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Humans
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Male
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Prostatic Diseases
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metabolism
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pathology
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Transient Receptor Potential Channels
7.Effects of power frequency magnetic field on Ca2+ transport of skeletal muscle sarcoplasmic reticulum vesicles.
Ren-chen LIU ; Zhen-jie ZHOU ; Ke-ping CHU ; Xiu-li LIU ; Shu-de CHEN ; Ruo-hong XIA
Chinese Journal of Preventive Medicine 2006;40(3):168-172
OBJECTIVETo investigate the effects of power frequency magnetic field on the Ca2+ transport dynamics of isolated sarcoplasmic reticulum vesicles.
METHODSThe assays of Ca2+ uptake time course and the Ca2+-ATPase activity of sarcoplasmic reticulum vesicles were investigated by using dynamic mode of spectrometry with a Ca2+ dye; Ca2+ release channel activation was examined by 3H-ryanodine binding and Ca2+ release assays; membrane fluidity of sarcoplasmic reticulum vesicles was examined by fluorescence polarization, without or with exposure to the vesicles at a 0.4 mT, 50 Hz sinusoidal magnetic field.
RESULTS0.4 mT, 50 Hz sinusoidal magnetic field exposure caused about a 16% decline of the initial Ca2+ uptake rate from a (29.18 +/- 3.90) pmol.mg(-1).s(-1) to a (24.60 +/- 3.81) pmol.mg(-1).s(-1) and a 26% decline of the Ca2+-ATPase activity from (0.93 +/- 0.05) micromol.mg(-1).min(-1) to (0.69 +/- 0.07) micromol.mg(-1).min(-1) of sarcoplasmic reticulum vesicles, whereas caused a 15% increase of the initial Ca2+ release rate from (4.83 +/- 0.82) pmol.mg(-1).s(-1) to (5.65 +/- 0.43) pmol.mg(-1).s(-1) and a 5% increase in 3H-ryanodine binding to the receptor from (1.10 +/- 0.12) pmol/mg to (1.16 +/- 0.13) pmol/mg, respectively.
CONCLUSIONThe decline of Ca2+-ATPase activity and the increase of Ca2+ release channel activity should result in a down-regulation of Ca2+ dynamic uptake and an up-regulation of Ca2+ release induced by exposing the sarcoplasmic reticulum to a 0.4 mT, 50 Hz power frequency magnetic field.
Animals ; Calcium ; metabolism ; Calcium Signaling ; Electromagnetic Fields ; Muscle, Skeletal ; metabolism ; Rabbits ; Sarcoplasmic Reticulum ; metabolism ; radiation effects
8.Regulation of voltage-gated calcium channels by proteolysis.
Acta Physiologica Sinica 2012;64(5):504-514
Voltage gated calcium channels (VGCCs) are multi-subunit membrane proteins present in a variety of tissues and control many essential physiological processes. Due to their vital importance, VGCCs are regulated by a myriad of proteins and signaling pathways. Here we review the literature on the regulation of VGCCs by proteolysis of the pore-forming α1 subunit, Ca(v)α(1). This form of regulation modulates channel function and degradation and affects cellular gene expression and excitability. L-type Ca(2+) channels are proteolyzed in two ways, depending on tissue localization. In the heart and skeletal muscle, the distal C-terminus of Ca(v)α(1) is cleaved and acts as an autoinhibitor when it reassociates with the proximal C-terminus. Relief of this autoinhibition underlies the β-adrenergic stimulation-induced enhancement of cardiac and skeletal muscle calcium currents, part of the "fight or flight" response. Proteolysis of the distal C-terminus of L-type channels also occurs in the brain and is probably catalyzed by a calpain-like protease. In some brain regions, the entire C-terminus of L-type Ca(2+) channels can be cleaved by an unknown protease and translocates to the nucleus acting as a transcription factor. The distal C-terminus of P/Q-channel Ca(v)α(1) is also proteolyzed and translocates to the nucleus. Truncated forms of the PQ-channel Ca(v)α(1) are produced by many disease-causing mutations and interfere with the function of full-length channels. Truncated forms of N-type channel Ca(v)α(1), generated by mutagenesis, affect the expression of full-length channels. New forms of proteolysis of VGCC subunits remain to be discovered and may represent a fruitful area of VGCC research.
Animals
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Calcium Channels, L-Type
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metabolism
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Calcium Signaling
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Humans
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Muscle, Skeletal
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physiology
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Proteolysis
9.Characteristics of free calcium distribution and Ca(2+) oscillations in the subregeon of hepatocytes.
Feng XIA ; Zhen Ping HE ; Kun LI ; Li CHEN ; Xiao Li WANG ; Jia Hong DONG
Chinese Journal of Hepatology 2003;11(2):119-119
Calcium
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metabolism
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Calcium Signaling
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Epinephrine
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pharmacology
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Hepatocytes
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drug effects
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metabolism
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Humans
10.TRPM7 Is Essential for RANKL-Induced Osteoclastogenesis.
Yu Mi YANG ; Hwi Hoon JUNG ; Sung Jun LEE ; Hyung Jun CHOI ; Min Seuk KIM ; Dong Min SHIN
The Korean Journal of Physiology and Pharmacology 2013;17(1):65-71
The transient receptor potential melastatin type 7 (TRPM7) channel is a widely expressed non-selective cation channel with fusion to the C-terminal alpha kinase domain and regarded as a key regulator of whole body Mg2+ homeostasis in mammals. However, the roles of TRPM7 during osteoclastogenesis in RAW264.7 cells and bone marrow-derived monocyte/macrophage precursor cells (BMMs) are not clear. In the present study, we investigate the roles of TRPM7 in osteoclastogenesis using methods of small interfering RNA (siRNA), RT-PCR, patch-clamp, and calcium imaging. RANKL (receptor activator of NF-kappaB ligand) stimulation did not affect the TRPM7 expression and TRPM7-mediated current was activated in HEK293, RAW264.7, and BMM cells by the regulation of Mg2+. Knock-down of TRPM7 by siTRPM7 reduced intracellular Ca2+ concentration ([Ca2+]i) increases by 0 mM [Mg2+]e in HEK293 cells and inhibited the generation of RANKL-induced Ca2+ oscillations in RAW264.7 cells. Finally, knock-down of TRPM7 suppressed RANKL-mediated osteoclastogenesis such as activation and translocation of NFATc1, formation of multinucleated cells, and the bone resorptive activity, sequentially. These results suggest that TRPM7 plays an essential role in the RANKL-induced [Ca2+]i oscillations that triggers the late stages of osteoclastogenesis.
Calcium
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Calcium Signaling
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HEK293 Cells
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Homeostasis
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Mammals
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NF-kappa B
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Phosphotransferases
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RNA, Small Interfering