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Specialty: Cytology
Nutrition: Calcium

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Total 42 results found since Jan 2013.

Human Umbilical Cord Mesenchymal Stem Cells Preserve Adult Newborn Neurons and Reduce Neurological Injury after Cerebral Ischemia by Reducing the Number of Hypertrophic Microglia/Macrophages.
Abstract Microglia are the first source of a neuroinflammatory cascade, which seems to be involved in every phase of stroke-related neuronal damage. Two weeks after transient middle cerebral artery occlusion (MCAO), vehicle-treated rats displayed higher numbers of total ionized calcium-binding adaptor molecule 1 (Iba-1)-positive cells, greater cell body areas of Iba-1-positive cells, and higher numbers of hypertrophic Iba-1-positive cells (with a cell body area over 80 μm2) in the ipsilateral ischemic brain regions including the frontal cortex, striatum, and parietal cortex. In addition, MCAO decreased the number...
Source: Cell Transplantation - November 1, 2017 Category: Cytology Authors: Lin W, Hsuan YC, Lin MT, Kuo TW, Lin CH, Su YC, Niu KC, Chang CP, Lin HJ Tags: Cell Transplant Source Type: research

Memantine Attenuates Cell Apoptosis by Suppressing the Calpain-Caspase-3 Pathway in an Experimental Model of Ischemic Stroke.
Abstract Ischemic stroke, the second leading cause of death worldwide, leads to excessive glutamate release, over-activation of N-methyl-D-aspartate receptor (NMDAR), and massive influx of calcium (Ca(2+)), which may activate calpain and caspase-3, resulting in cellular damage and death. Memantine is an uncompetitive NMDAR antagonist with low-affinity/fast off-rate. We investigated the potential mechanisms through which memantine protects against ischemic stroke in vitro and in vivo. Middle cerebral artery occlusion-reperfusion (MCAO) was performed to establish an experimental model of ischemic stroke. The neuropr...
Source: Experimental Cell Research - January 5, 2017 Category: Cytology Authors: Chen B, Wang G, Li W, Liu W, Lin R, Tao J, Jiang M, Chen L, Wang Y Tags: Exp Cell Res Source Type: research

Biphasic regulation of lysosomal exocytosis by oxidative stress.
Abstract Oxidative stress drives cell death in a number of diseases including ischemic stroke and neurodegenerative diseases. A better understanding of how cells recover from oxidative stress is likely to lead to better treatments for stroke and other diseases. The recent evidence obtained in several models ties the process of lysosomal exocytosis to the clearance of protein aggregates and toxic metals. The mechanisms that regulate lysosomal exocytosis, under normal or pathological conditions, are only beginning to emerge. Here we provide evidence for the biphasic effect of oxidative stress on lysosomal exocytosis...
Source: Cell Calcium - August 28, 2016 Category: Cytology Authors: Ravi S, Peña KA, Chu CT, Kiselyov K Tags: Cell Calcium Source Type: research

Gene Polymorphisms Affect the Effectiveness of Atorvastatin in Treating Ischemic Stroke Patients
Background/Aims: The aim of the present study is to investigate whether the single nucleotide polymorphism (SNP) in lipid metabolism related genes would affect the effectiveness of atorvastatin in both Han and Uighur populations. Methods: 200 ischemic stroke patients were treated with atorvastatin. The differences of blood lipid level and their ratios were measured. Six lipid related genes, HMGCR, APOA5, LPL, CETP, LDLR and PCSK9 were selected as candidate genes. And nine SNP loci in these six genes were genotyped by SNaPshot technique. Results: In all patients treated with atorvastatin, the SNP rs662799 significantly affe...
Source: Cellular Physiology and Biochemistry - July 14, 2016 Category: Cytology Source Type: research

ROS and intracellular ion channels.
Abstract Oxidative stress is a well-known driver of numerous pathological processes involving protein and lipid peroxidation and DNA damage. The resulting increase of pro-apoptotic pressure drives tissue damage in a host of conditions, including ischemic stroke and reperfusion injury, diabetes, death in acute pancreatitis and neurodegenerative diseases. Somewhat less frequently discussed, but arguably as important, is the signaling function of oxidative stress stemming from the ability of oxidative stress to modulate ion channel activity. The evidence for the modulation of the intracellular ion channels and transp...
Source: Cell Calcium - March 10, 2016 Category: Cytology Authors: Kiselyov K, Muallem S Tags: Cell Calcium Source Type: research

EP3, Prostaglandin E2 Receptor Subtype 3, Associated with Neuronal Apoptosis Following Intracerebral Hemorrhage.
Abstract EP3 is prostaglandin E2 receptor subtype 3 and mediates the activation of several signaling pathways, changing in cAMP levels, calcium mobilization, and activation of phospholipase C. Previous studies demonstrated a direct role for EP3 in various neurodegenerative disorders, such as stroke and Alzheimer disease. However, the distribution and function of EP3 in ICH diseases remain unknown. Here, we demonstrate that EP3 may be involved in neuronal apoptosis in the processes of intracerebral hemorrhage (ICH). From the results of Western blot and immunohistochemistry, we obtained a significant up-regulation o...
Source: Cellular and Molecular Neurobiology - December 30, 2015 Category: Cytology Authors: Ni H, Shen J, Song Y, Cao M, Liu X, Huang J, Zhang W, Xie L, Ning X, Ke K Tags: Cell Mol Neurobiol Source Type: research

Disruption of IP3R2-mediated Ca(2+) signaling pathway in astrocytes ameliorates neuronal death and brain damage while reducing behavioral deficits after focal ischemic stroke.
Abstract Inositol trisphosphate receptor (IP3R)-mediated intracellular Ca(2+) increase is the major Ca(2+) signaling pathway in astrocytes in the central nervous system (CNS). Ca(2+) increases in astrocytes have been found to modulate neuronal function through gliotransmitter release. We previously demonstrated that astrocytes exhibit enhanced Ca(2+) signaling in vivo after photothrombosis (PT)-induced ischemia, which is largely due to the activation of G-protein coupled receptors (GPCRs). The aim of this study is to investigate the role of astrocytic IP3R-mediated Ca(2+) signaling in neuronal death, brain damage ...
Source: Cell Calcium - September 25, 2015 Category: Cytology Authors: Li H, Xie Y, Zhang N, Yu Y, Zhang Q, Ding S Tags: Cell Calcium Source Type: research

The Noncompetitive AMPAR Antagonist Perampanel Abrogates Brain Endothelial Cell Permeability in Response to Ischemia: Involvement of Claudin-5.
Abstract The blood-brain barrier (BBB) is formed by brain endothelial cells, and decreased BBB integrity contributes to vasogenic cerebral edema and increased mortality after stroke. In the present study, we investigated the protective effect of perampanel, an orally active noncompetitive AMPA receptor antagonist, on BBB permeability in an in vitro ischemia model in murine brain endothelial cells (mBECs). The results showed that perampanel significantly attenuated oxygen glucose deprivation (OGD)-induced loss of cell viability, release of lactate dehydrogenase, and apoptotic cell death in a dose-dependent manner. ...
Source: Cellular and Molecular Neurobiology - August 26, 2015 Category: Cytology Authors: Lv JM, Guo XM, Chen B, Lei Q, Pan YJ, Yang Q Tags: Cell Mol Neurobiol Source Type: research

BDNF Reduces Toxic Extrasynaptic NMDA Receptor Signaling via Synaptic NMDA Receptors and Nuclear-Calcium-Induced Transcription of inhba/Activin A
Publication date: Available online 13 August 2015 Source:Cell Reports Author(s): David Lau, C. Peter Bengtson, Bettina Buchthal, Hilmar Bading The health of neurons is critically dependent on the relative signaling intensities of survival-promoting synaptic and death-inducing extrasynaptic NMDA receptors. Here, we show that BDNF is a regulator of this balance and promotes neuroprotection by reducing toxic NMDA receptor signaling. BDNF acts by initiating synaptic NMDA-receptor/nuclear-calcium-driven adaptogenomics, leading to increased expression of inhibin β-A (inhba). Inhibin β-A (its homodimer is known as activi...
Source: Cell Reports - August 14, 2015 Category: Cytology Source Type: research

NH2-terminal truncations of cardiac troponin I and cardiac troponin T produce distinct effects on contractility and calcium homeostasis in adult cardiomyocytes
Cardiac troponin I (TnI) has an NH2-terminal extension that is an adult heart-specific regulatory structure. Restrictive proteolytic truncation of the NH2-terminal extension of cardiac TnI occurs in normal hearts and is upregulated in cardiac adaptation to hemodynamic stress or β-adrenergic deficiency. NH2-terminal truncated cardiac TnI (cTnI-ND) alters the conformation of the core structure of cardiac TnI similarly to that produced by PKA phosphorylation of Ser23/24 in the NH2-terminal extension. At organ level, cTnI-ND enhances ventricular diastolic function. The NH2-terminal region of cardiac troponin T (TnT) is an...
Source: AJP: Cell Physiology - March 1, 2015 Category: Cytology Authors: Wei, H., Jin, J.- P. Tags: ARTICLES Source Type: research

N-terminal truncations of cardiac troponin I and cardiac troponin T produce distinct effects on contractility and calcium homeostasis in adult cardiomyocytes.
Abstract Cardiac troponin I (TnI) has an N-terminal extension that is an adult heart-specific regulatory structure. Restrictive proteolytic truncation of the N-terminal extension of cardiac TnI occurs in normal hearts and is up-regulated in cardiac adaptation to hemodynamic stress or β-adrenergic deficiency. N-terminal truncated cardiac TnI (cTnI-ND) alters the conformation of the core structure of cardiac TnI, similarly to that produced by PKA phosphorylation of Ser23/24 in the N-terminal extension. At organ level, cTnI-ND enhances ventricular diastolic function. The N-terminal region of cardiac troponin T (TnT)...
Source: American Journal of Physiology. Cell Physiology - December 17, 2014 Category: Cytology Authors: Wei H, Jin JP Tags: Am J Physiol Cell Physiol Source Type: research

The inhibitory effect of simvastatin and aspirin on histamine responsiveness in human vascular endothelial cells
Statins and aspirin deliver well-established cardiovascular benefits resulting in their increased use as combined polypills to decrease risk of stroke and heart disease. However, the direct endothelial effect of combined statin/aspirin cotreatment remains unclear. Histamine is an inflammatory mediator that increases vascular permeability, and so we examined the effect of treating human umbilical vein endothelial cells (HUVECs) for 24 h with 1 μM simvastatin and 100 μM aspirin on histamine responsiveness. Subsequent histamine (1 μM) challenge increased intracellular calcium (Ca2+i) concentration, an effect that was...
Source: AJP: Cell Physiology - April 1, 2014 Category: Cytology Authors: Absi, M., Bruce, J. I., Ward, D. T. Tags: ARTICLES Source Type: research