NDLI: Blocking mPTP on Neural Stem Cells and Activating the Nicotinic Acetylcholine Receptor α7 Subunit on Microglia Attenuate Aβ-Induced Neurotoxicity on Neural Stem Cells

Please wait, while we are loading the content...

Heat shock protein 60 affects behavioral improvement in a rat model of Parkinson’s disease grafted with human umbilical cord mesenchymal stem cell-derived dopaminergic-like neurons

Mitochondrial Ca$^{2+}$ Processing by a Unit of Mitochondrial Ca$^{2+}$ Uniporter and Na$^{+}$/Ca$^{2+}$ Exchanger Supports the Neuronal Ca$^{2+}$ Influx via Activated Glutamate Receptors

Upregulated P2X3 Receptor Expression in Patients with Intractable Temporal Lobe Epilepsy and in a Rat Model of Epilepsy

The Administration of Levocabastine, a NTS2 Receptor Antagonist, Modifies Na$^{+}$, K$^{+}$-ATPase Properties

Effects of High Glucose on Cell Viability and Differentiation in Primary Cultured Schwann Cells: Potential Role of ERK Signaling Pathway

β-Caryophyllene Attenuates Focal Cerebral Ischemia-Reperfusion Injury by Nrf2/HO-1 Pathway in Rats

CX3CR1-Mediated Akt1 Activation Contributes to the Paclitaxel-Induced Painful Peripheral Neuropathy in Rats

CXCL12/CXCR4 Axis Improves Migration of Neuroblasts Along Corpus Callosum by Stimulating MMP-2 Secretion After Traumatic Brain Injury in Rats

Protective Effects of Paeoniflorin Against MPP$^{+}$-induced Neurotoxicity in PC12 Cells

Mdivi-1 Protects Epileptic Hippocampal Neurons from Apoptosis via Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress in Vitro

Salicylate-Induced Hearing Loss Trigger Structural Synaptic Modifications in the Ventral Cochlear Nucleus of Rats via Medial Olivocochlear (MOC) Feedback Circuit

Lycopene Prevents Amyloid [Beta]-Induced Mitochondrial Oxidative Stress and Dysfunctions in Cultured Rat Cortical Neurons

Effect of the Anti-depressant Sertraline, the Novel Anti-seizure Drug Vinpocetine and Several Conventional Antiepileptic Drugs on the Epileptiform EEG Activity Induced by 4-Aminopyridine

Intranasal Delivery of Recombinant NT4-NAP/AAV Exerts Potential Antidepressant Effect

Endogenous CBS–H$_{2}$S Pathway Contributes to the Development of CCI-Induced Neuropathic Pain

A Pit-1 Binding Site Adjacent to E-box133 in the Rat PRL Promoter is Necessary for Pulsatile Gene Expression Activity

Gastrodin Attenuates Cognitive Deficits Induced by 3,3′-Iminodipropionitrile

Morphine Inhibited the Rat Neural Stem Cell Proliferation Rate by Increasing Neuro Steroid Genesis

Insulin Stimulates S100B Secretion and These Proteins Antagonistically Modulate Brain Glucose Metabolism

Diphenyl Diselenide Protects Against Mortality, Locomotor Deficits and Oxidative Stress in Drosophila melanogaster Model of Manganese-Induced Neurotoxicity

Induction of S-Phase Arrest in Human Glioma Cells by Selenocysteine, a Natural Selenium-Containing Agent Via Triggering Reactive Oxygen Species-Mediated DNA Damage and Modulating MAPKs and AKT Pathways

Lipopolysaccharide Upregulates the Expression of CINC-3 and LIX in Primary NG2 Cells

The Neuroprotective Effects of Justicidin A on Amyloid Beta$_{25–35}$-Induced Neuronal Cell Death Through Inhibition of Tau Hyperphosphorylation and Induction of Autophagy in SH-SY5Y Cells

Chronic (3-Weeks) Treatment of Estrogen (17β-Estradiol) Enhances Working and Reference Memory in Ovariectomized Rats: Role of Acetylcholine

Kinetics and Molecular Docking Study of an Anti-diabetic Drug Glimepiride as Acetylcholinesterase Inhibitor: Implication for Alzheimer’s Disease-Diabetes Dual Therapy

Blocking mPTP on Neural Stem Cells and Activating the Nicotinic Acetylcholine Receptor α7 Subunit on Microglia Attenuate Aβ-Induced Neurotoxicity on Neural Stem Cells

Rutin Inhibits Neuroinflammation and Provides Neuroprotection in an Experimental Rat Model of Subarachnoid Hemorrhage, Possibly Through Suppressing the RAGE–NF-κB Inflammatory Signaling Pathway

Retraction Note to: Up-Regulation of KPNB1 Involves in Neuronal Apoptosis Following Intracerebral Hemorrhage in Adult Rats

Neurochemical Research : Volume 41, Issue 5, May 2016

Neurochemical Research : Volume 41, Issue 4, April 2016

Neurochemical Research : Volume 41, Issue 3, March 2016

Neurochemical Research : Volume 41, Issue 1-2, February 2016

Neurochemical Research : Volume 40

Neurochemical Research : Volume 39

Neurochemical Research : Volume 38

Neurochemical Research : Volume 37

Neurochemical Research : Volume 36

Neurochemical Research : Volume 35

Neurochemical Research : Volume 34

Neurochemical Research : Volume 33

Neurochemical Research : Volume 32

Neurochemical Research : Volume 31

Neurochemical Research : Volume 30

Neurochemical Research : Volume 29

Neurochemical Research : Volume 28

Neurochemical Research : Volume 27

Neurochemical Research : Volume 26

Neurochemical Research : Volume 25

Neurochemical Research : Volume 24

Neurochemical Research : Volume 23

Neurochemical Research : Volume 22

Blocking mPTP on Neural Stem Cells and Activating the Nicotinic Acetylcholine Receptor α7 Subunit on Microglia Attenuate Aβ-Induced Neurotoxicity on Neural Stem Cells

Content Provider	Springer Nature Link
Author	Chen, Qingzhuang Wang, Kewan Jiang, Deqi Wang, Yan Xiao, Xiaodan Zhu, Ning Li, Mingxing Jia, Siyuan Wang, Yong
Copyright Year	2016
Abstract	β-Amyloid (Aβ) can stimulate microglia to release a variety of proinflammatory cytokines and induce neurotoxicity. Nicotine has been reported to inhibit TNF-α, IL-1, and ROS production in microglia. Mitochondrial permeability transition pore (mPTP) plays an important role in neurotoxicity as well. Here, we investigated whether activating the microglial α7-nAChR has a neuroprotective role on neural stem cells (NSCs) and the function of mPTP in NSCs in this process. The expression of α7-nAChR in rat NSCs was detected by immunocytochemistry and RT-PCR. The viability of microglia and NSCs was examined by MTT assay. The mitochondrial membrane potential (ΔΨm) and morphological characteristics of NSCs was measured by JC-1 staining and transmission electron microscopy respectively. The distribution of cytochrome c in the subcellular regions of NSCs was visualized by confocal laser scanning microscopy, and the expression levels of cyclophilin D and cleaved caspase-3 were assayed by western blot. The apoptotic rate of NSCs was measured by flow cytometry. The expression of α7-nAChR was detected in microglial cells, but no expression was found in NSCs. The viability of rat microglial cells and NSCs was not affected by reagents or coculture itself. Aβ$_{1–42}$-mediated microglial activation impaired the morphology and the ΔΨm of mitochondria of NSCs as well as increased cell apoptosis. However, the damage was attenuated when the α7-nAChRs on microglial cells were activated or the mPTPs on NSCs were blocked. Blockade of mPTPs on NSCs and activation of α7-nAChRs on microglia exhibit neuroprotective roles in Aβ-induced neurotoxicity of NSCs.
Starting Page	1483
Ending Page	1495
Page Count	13
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	41
Issue Number	6
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2016-02-15
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Mitochondrial permeability transition pore Microglia Neural stem cells Inflammatory response β-Amyloid Nicotinic acetylcholine receptor α7 subunit Neurosciences Neurochemistry Biochemistry Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Preventing Expression of the Nicotinic Receptor Subunit α7 in SH-SY5Y Cells with Interference RNA Indicates that this Receptor may Protect Against the Neurotoxicity of Aβ

Nicotine Prevents Synaptic Impairment Induced by Amyloid-β Oligomers Through α7-Nicotinic Acetylcholine Receptor Activation

Possible Effect of Activation of α7-Nicotinic Acetylcholine Receptors in the Mitochondrial Membrane on the Development of Apoptosis

The spinal microglial IL-10/β-endorphin pathway accounts for cinobufagin-induced mechanical antiallodynia in bone cancer pain following activation of α7-nicotinic acetylcholine receptors

β-Amyloid Peptide Activates α7 Nicotinic Acetylcholine Receptors Expressed in Xenopus Oocytes

α7 nicotinic acetylcholine receptor-mediated neuroprotection against dopaminergic neuron loss in an MPTP mouse model via inhibition of astrocyte activation

α7 nicotinic acetylcholine receptor signaling modulates the inflammatory and iron homeostasis in fetal brain microglia

Overexpression of mitochondrial Hsp75 protects neural stem cells against microglia-derived soluble factor-induced neurotoxicity by regulating mitochondrial permeability transition pore opening in vitro

Short-Term High-Fat Diet Consumption Reduces Hypothalamic Expression of the Nicotinic Acetylcholine Receptor α7 Subunit (α7nAChR) and Affects the Anti-inflammatory Response in a Mouse Model of Sepsis

Blocking mPTP on Neural Stem Cells and Activating the Nicotinic Acetylcholine Receptor α7 Subunit on Microglia Attenuate Aβ-Induced Neurotoxicity on Neural Stem Cells

Similar Documents

Preventing Expression of the Nicotinic Receptor Subunit α7 in SH-SY5Y Cells with Interference RNA Indicates that this Receptor may Protect Against the Neurotoxicity of Aβ

Nicotine Prevents Synaptic Impairment Induced by Amyloid-β Oligomers Through α7-Nicotinic Acetylcholine Receptor Activation

Possible Effect of Activation of α7-Nicotinic Acetylcholine Receptors in the Mitochondrial Membrane on the Development of Apoptosis

The spinal microglial IL-10/β-endorphin pathway accounts for cinobufagin-induced mechanical antiallodynia in bone cancer pain following activation of α7-nicotinic acetylcholine receptors

β-Amyloid Peptide Activates α7 Nicotinic Acetylcholine Receptors Expressed in Xenopus Oocytes

α7 nicotinic acetylcholine receptor-mediated neuroprotection against dopaminergic neuron loss in an MPTP mouse model via inhibition of astrocyte activation

α7 nicotinic acetylcholine receptor signaling modulates the inflammatory and iron homeostasis in fetal brain microglia

Overexpression of mitochondrial Hsp75 protects neural stem cells against microglia-derived soluble factor-induced neurotoxicity by regulating mitochondrial permeability transition pore opening in vitro

Short-Term High-Fat Diet Consumption Reduces Hypothalamic Expression of the Nicotinic Acetylcholine Receptor α7 Subunit (α7nAChR) and Affects the Anti-inflammatory Response in a Mouse Model of Sepsis

Blocking mPTP on Neural Stem Cells and Activating the Nicotinic Acetylcholine Receptor α7 Subunit on Microglia Attenuate Aβ-Induced Neurotoxicity on Neural Stem Cells