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Specialty: Neurology

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Total 636 results found since Jan 2013.

Downregulation of RTN1-C attenuates MPP+-induced neuronal injury through inhibition of mGluR5 pathway in SN4741 cells.
In conclusion, our data suggest that downregulation of RTN1-C protects SN4741 cells against MPP+ through mGluR5-mediated preservation of Ca2+ homeostasis. Therefore, RTN1-C might represent a therapeutic target for the treatment of neuronal injury in experimental PD models. PMID: 30521940 [PubMed - as supplied by publisher]
Source: Brain Research Bulletin - December 3, 2018 Category: Neurology Authors: Chang J, Zhang XL, Yu H, Chen J Tags: Brain Res Bull Source Type: research

Alpha-naphthoflavone induces apoptosis through endoplasmic reticulum stress via c-Src-, ROS-, MAPKs-, and arylhydrocarbon receptor-dependent pathways in HT22 hippocampal neuronal cells.
Abstract α-Naphthoflavone (αNF) is a prototype flavone, also known as a modulator of aryl hydrocarbon receptor (AhR). In the present study, we investigated the molecular mechanisms of αNF-induced cytotoxic effects in HT22 mouse hippocampal neuronal cells. αNF induced apoptotic cell death via activation of caspase-12 and -3 and increased expression of endoplasmic reticulum (ER) stress-associated proteins, including C/EBP homologous protein (CHOP). Inhibition of ER stress by treatment with the ER stress inhibitor, salubrinal, or by CHOP siRNA transfection reduced αNF-induced cell death. αNF activated mitogen-a...
Source: Neurotoxicology - November 30, 2018 Category: Neurology Authors: Yu AR, Ju Jeong Y, Hwang CY, Yoon KS, Choe W, Ha J, Kim SS, Kim Pak Y, Yeo EJ, Kang I Tags: Neurotoxicology Source Type: research

Resveratrol treatment reduces the vulnerability of SH-SY5Y cells and cortical neurons overexpressing SOD1-G93A to Thimerosal toxicity through SIRT1/DREAM/PDYN pathway.
Abstract In humans, mutation of glycine 93 to alanine of Cu++/Zn++ superoxide dismutase type-1 (SOD1-G93 A) has been associated to some familial cases of Amyotrophic Lateral Sclerosis (ALS). Several evidence proposed the involvement of environmental pollutants that like mercury could accelerate ALS symptoms. SH-SY5Y cells stably transfected with SOD1 and G93 A mutant of SOD1 constructs were exposed to non-toxic concentrations (0.01 µM) of ethylmercury thiosalicylate (thimerosal) for 24 hours. Interestingly, we found that thimerosal, in SOD1-G93 A cells, but not in SOD1 cells, reduced cell survival. Furthe...
Source: Neurotoxicology - November 29, 2018 Category: Neurology Authors: Laudati G, Mascolo L, Guida N, Sirabella R, Pizzorusso V, Bruzzaniti S, Serani A, Di Renzo G, Canzoniero LM, Formisano L Tags: Neurotoxicology Source Type: research

Forced FoxO1:S249V expression suppressed glioma cell proliferation through G2/M cell cycle arrests and increased apoptosis.
CONCLUSION: Our findings suggest that the forced FoxO1:S249V suppressed the cell growth through G2/M cell cycle arrests and increased apoptosis in glioma. PMID: 30453847 [PubMed - as supplied by publisher]
Source: Neurological Research - November 22, 2018 Category: Neurology Tags: Neurol Res Source Type: research

Mammalian Target of Rapamycin Complex 1 Activation Disrupts the Low-Density Lipoprotein Receptor Pathway: A Novel Mechanism for Extracellular Matrix Accumulation in Human Peritoneal Mesothelial Cells
Peritoneal fibrosis (PF) is characterized by progressive extracellular matrix (ECM) accumulation. Increasing evidence has suggested that ECM synthesis was increased in human peritoneal mesothelial cells (HPMCs) under high-glucose conditions, but the effects of high-glucose peritoneal dialysis solution (PDS) on ECM synthesis have not been fully elucidated. The aim of this study was to explore the potential mechanisms of high-glucose PDS-induced production of ECM in  HPMCs. HPMCs were stimulated by high-glucose PDS. The activity of mammalian target of rapamycin complex 1 (mTORC1) was inhibited by rapamycin or regulatory-as...
Source: American Journal of Nephrology - November 13, 2018 Category: Neurology Source Type: research

Hypoxia enhances the migration and invasion of human glioblastoma U87 cells through PI3K/Akt/mTOR/HIF-1α pathway
This study aims to explore the role of phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway and its relationship with hypoxia inducible factor-1α (HIF-1α) in the migration and invasion of human glioblastoma U87 cells under hypoxia. In the study, we found that hypoxia could activate the PI3K/Akt/mTOR pathway associated with the enhancements of the migration and invasion of human glioblastoma U87 cells. When the PI3K/Akt/mTOR pathway and HIF-1α were inhibited by the siRNAs or inhibitors, the migration and invasion of human glioblastoma U87 cells were suppressed. Meanwhile, t...
Source: NeuroReport - November 9, 2018 Category: Neurology Tags: CELLULAR, MOLECULAR AND DEVELOPMENTAL NEUROSCIENCE Source Type: research

FOXRED1 silencing in mice: a possible animal model for Leigh syndrome
AbstractLeigh syndrome (LS) is one of the most puzzling mitochondrial disorders, which is also known as subacute necrotizing encephalopathy. It has an incidence of 1 in 77,000 live births worldwide with poor prognosis. Currently, there is a poor understanding of the underlying pathophysiological mechanisms of the disease without any available effective treatment. Hence, the inevitability for developing suitable animal and cellular models needed for the development of successful new therapeutic modalities. In this short report, we blocked FOXRED1 gene with small interfering RNA (siRNA) using C57bl/6 mice. Results showed neu...
Source: Metabolic Brain Disease - November 3, 2018 Category: Neurology Source Type: research

A Mesenchymal stem cell line (B10) increases angiogenesis in a rat MCAO model.
Abstract A human mesenchymal stem cell line (B10) transplantation has been shown to improve ischemia-induced neurological deficits in animal stroke models. To understand the underlying mechanism, we have investigated the effects of B10 transplantation on cerebral angiogenesis in a rat middle cerebral artery occlusion (MCAO) model. B10 cells were transplanted intravenously 24 h after MCAO. Immunofluorescence staining results showed that compared to PBS-groups, vWF positive vessel and endoglin positive new vessels were increased in B10-transplanted MCAO groups in the lesion areas. The mRNA of angiogenesis factors ...
Source: Experimental Neurology - October 3, 2018 Category: Neurology Authors: Sheikh AM, Yano S, Mitaki S, Haque MA, Yamaguchi S, Nagai A Tags: Exp Neurol Source Type: research

Coconut Oil Decreases Expression of Amyloid Precursor Protein (APP) and Secretion of Amyloid Peptides throughInhibitionof ADP-ribosylation factor 1 (ARF1).
CONCLUSION: These results suggest that coconut oil decreases intracellular ARF1 expression, thereby resulting in an inhibition of APP and amyloid β secretion. This study reveals a novel mechanism for intracellular APP processing in neuronal cells. PMID: 30287345 [PubMed - as supplied by publisher]
Source: Brain Research - October 1, 2018 Category: Neurology Authors: Bansal A, Kirschner M, Zu L, Cai D, Zhang L Tags: Brain Res Source Type: research

Evidence that NLRC4 Inflammasome Mediates Apoptotic and Pyroptotic Microglial Death Following Ischemic Stroke
This study has comprehensively investigated the expression and activation of NLRP1, NLRP3, NLRC4 and AIM2 inflammasomes in isolates of microglial cells subjected to simulated ischemic conditions and in the brain following ischemic stroke. Immunoblot analysis from culture media indicated microglial cells release inflammasome components and inflammasome activation-dependent pro-inflammatory cytokines following ischemic conditions. In addition, a functional role for NLRC4 inflammasomes was determined using siRNA knockdown of NLRC4 and pharmacological inhibitors of caspase-1 and -8 to target apoptotic and pyroptotic cell death...
Source: Brain, Behavior, and Immunity - September 6, 2018 Category: Neurology Source Type: research

Evidence that NLRC4 Inflammasome Mediates Apoptotic and Pyroptotic Microglial Death Following Ischemic Stroke.
This study has comprehensively investigated the expression and activation of NLRP1, NLRP3, NLRC4 and AIM2 inflammasomes in isolates of microglial cells subjected to simulated ischemic conditions and in the brain following ischemic stroke. Immunoblot analysis from culture media indicated microglial cells release inflammasome components and inflammasome activation-dependent pro-inflammatory cytokines following ischemic conditions. In addition, a functional role for NLRC4 inflammasomes was determined using siRNA knockdown of NLRC4 and pharmacological inhibitors of caspase-1 and -8 to target apoptotic and pyroptotic cell death...
Source: Brain, Behavior, and Immunity - September 5, 2018 Category: Neurology Authors: Poh L, Kang SW, Baik SH, Yong Quan Ng G, She DT, Balaganapathy P, Thameem Dheen S, Magnus T, Gelderblom M, Sobey CG, Koo EH, Fann DY, Arumugam TV Tags: Brain Behav Immun Source Type: research

Identification of the biological affection of long noncoding RNA BC200 in Alzheimer’s disease
BC200 is a long noncoding RNA expressed at high levels in the Alzheimer’s disease (AD), and blocking of BC200 by siRNA is assumed to be an effective method for various disease therapy. We have established an AD cell model overexpressing amyloid β-peptide (Aβ)1-42 to observe the effects of BC200 on the cell viability and apoptosis, and to investigate the associated underlying mechanisms. Efficient knockdown and overexpression of BC200 were established using BC200 siRNA and BC200 mimics, respectively. Cell viability following BC200 knockdown and overexpression was assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenylte...
Source: NeuroReport - August 3, 2018 Category: Neurology Tags: Degeneration and Repair Source Type: research

LanCL1 attenuates ischemia-induced oxidative stress by Sirt3-mediated preservation of mitochondrial function.
Abstract Lanthionine synthetase C-like protein 1 (LanCL1) is homologous to prokaryotic lanthionine cyclases, and has been shown to have novel functions in neuronal redox homeostasis. A recent study showed that LanCL1 expression was developmental and activity-dependent regulated, and LanCL1 transgene protected neurons against oxidative stress. In the present study, the potential protective effects of LanCL1 against ischemia was investigated in an in vitro model mimicked by oxygen and glucose deprivation (OGD) in neuronal HT22 cells. We found that OGD exposure induced a temporal increase and persistent decreases in ...
Source: Brain Research Bulletin - July 31, 2018 Category: Neurology Authors: Xie Z, Cao BQ, Wang T, Lei Q, Kang T, Ge CY, Gao WJ, Hui H Tags: Brain Res Bull Source Type: research

Inhibition of immunoproteasome promotes angiogenesis via enhancing hypoxia-inducible factor-1α abundance in rats following focal cerebral ischaemia
In this study, we identified that inhibition of immunoproteasome LMP2 was able to enhance angiogenesis and facilitate neurological functional recovery in rats after focal cerebral ischemia/reperfusion. In vitro, oxygen-glucose deprivation and reperfusion (OGD/R) significantly enhanced the expression of immunoproteasome LMP2 and proteasome activities in primary culture astrocytes, but these beneficial effects were abolished by knockdown of LMP2 with siRNA transfection. Along with this, protein abundance of HIF-1α was significantly increased by inhibition LMP2 in vivo and in vitro and was associated with angiogenesis and ce...
Source: Brain, Behavior, and Immunity - July 11, 2018 Category: Neurology Source Type: research

Inhibition of the Nrf2/HO-1 Axis Suppresses the Mitochondria-Related Protection Promoted by Gastrodin in Human Neuroblastoma Cells Exposed to Paraquat
AbstractMitochondria are double-membrane organelles involved in the transduction of energy from different metabolic substrates into adenosine triphosphate (ATP) in mammalian cells. The oxidative phosphorylation system is comprised by the activity of the respiratory chain and the complex V (ATP synthase/ATPase). This system is dependent on oxygen gas (O2) in order to maintain a flux of electrons in the respiratory chain, since O2 is the final acceptor of these electrons. Electron leakage from this complex system leads to the continuous generation of reactive species in the cells. The mammalian cells exhibit certain mechanis...
Source: Molecular Neurobiology - July 11, 2018 Category: Neurology Source Type: research