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Sprouty2 —a Novel Therapeutic Target in the Nervous System?
AbstractClinical trials applying growth factors to alleviate symptoms of patients with neurological disorders have largely been unsuccessful in the past. As an alternative approach, growth factor receptors or components of their signal transduction machinery may be targeted directly. In recent years, the search for intracellular signaling integrator downstream of receptor tyrosine kinases provided valuable novel substrates. Among them are the Sprouty proteins which mainly act as inhibitors of growth factor-dependent neuronal and glial signaling pathways. In this review, we summarize the role of Sprouties in the lesioned ce...
Source: Molecular Neurobiology - May 7, 2019 Category: Neurology Source Type: research

A Parkinson's disease gene, DJ-1, regulates anti-inflammatory roles of astrocytes through prostaglandin D2 synthase expression.
Abstract Dysfunctional regulation of inflammation may contribute to the progression of neurodegenerative diseases. The results of this study revealed that DJ-1, a Parkinson's disease (PD) gene, regulated expression of prostaglandin D2 synthase (PTGDS) and production of prostaglandin D2 (PGD2), by which DJ-1 enhanced anti-inflammatory function of astrocytes. In injured DJ-1 knockout (KO) brain, expression of tumor necrosis factor-alpha (TNF-α) was more increased, but that of anti-inflammatory heme oxygenase-1 (HO-1) was less increased compared with that in injured wild-type (WT) brain. Similarly, astrocyte-conditi...
Source: Neurobiology of Disease - April 3, 2019 Category: Neurology Authors: Choi DJ, An J, Jou I, Park SM, Joe EH Tags: Neurobiol Dis Source Type: research

rh-IFN-α Attenuates Neuroinflammation and Improves Neurological Function by Inhibiting NF-κB through JAK1-STAT1/TRAF3 Pathway in an Experimental GMH Rat Model
In conclusion, our findings demonstrated that rh-IFN-α treatment attenuated neuroinflammation, neurological deficits and hydrocephalus formation through inhibiting microglial activation after GMH, which might be mediated by IFNAR/JAK1-STAT1/TRAF3/NF-κB signaling pathway. Rh-IFN-α may be a promising therapeutic agent to attenuate brain injury via its anti-inflammatory effect.
Source: Brain, Behavior, and Immunity - February 1, 2019 Category: Neurology Source Type: research

CK2 inhibition confers functional protection to young and aging axons against ischemia by differentially regulating the CDK5 and AKT signaling pathways.
Abstract White matter (WM) is injured in most strokes, which contributes to functional deficits during recovery. Casein kinase 2 (CK2) is a protein kinase that is expressed in brain, including WM. To assess the impact of CK2 inhibition on axon recovery following oxygen glucose deprivation (OGD), mouse optic nerves (MONs), which are pure WM tracts, were subjected to OGD with or without the selective CK2 inhibitor CX-4945. CX-4945 application preserved axon function during OGD and promoted axon function recovery when applied before or after OGD. This protective effect of CK2 inhibition correlated with preservation o...
Source: Neurobiology of Disease - June 23, 2018 Category: Neurology Authors: Bastian C, Quinn J, Tripathi A, Aquila D, Dutta AMR, Baltan S, Brunet S Tags: Neurobiol Dis Source Type: research

MicroRNA-499a decelerates glioma cell proliferation while accelerating apoptosis through the suppression of Notch1 and the MAPK signaling pathway.
Abstract As the most common and lethal of intracranial tumors, glioma accounts for 81% of all malignant brain tumors. Research data has identified the role of microRNAs (miRs) as functional suppressers in the progression of Glioma. The present study aimed to, ascertain as to whether microRNA-499a (miR-499a) influences cell proliferation and apoptosis through the MAPK signaling pathway by targeting Notch1 in glioma. Both glioma and adjacent tissues between 2012~2016, were obtained from People's Hospital of Zhengzhou University (Henan Provincial People's Hospital). The collected glioma cells were treated with miR-44...
Source: Brain Research Bulletin - June 14, 2018 Category: Neurology Authors: Wang BQ, Yang B, Yang HC, Wang JY, Hu S, Gao YS, Bu XY Tags: Brain Res Bull Source Type: research

AKAP150 involved in paclitaxel-induced neuropathic pain via inhibiting CN/NFAT2 pathway and downregulating IL-4
In this study, we found that A-kinase anchor protein 150 (AKAP150) was significantly upregulated after paclitaxel injection. Inhibition of AKAP150 via siRNA or AKAP150flox/flox in rodents alleviated the pain behavior induced by paclitaxel, and partly restored the decreased calcineurin (CN) phosphatase activity after paclitaxel treatment. Paclitaxel decreased the expression of anti-inflammatory cytokine interleukin-4 (IL-4), and intrathecal injections of IL-4 effectively alleviated paclitaxel-induced hypersensitivity and the frequency of dorsal root ganglion (DRG) neurons action potential. The decreased CN enzyme activity, ...
Source: Brain, Behavior, and Immunity - January 11, 2018 Category: Neurology Source Type: research

AKAP150 involved in Paclitaxel-Induced Neuropathic Pain via Inhibiting CN/NFAT2 pathway and downregulating IL-4.
In this study, we found that A-kinase anchor protein 150 (AKAP150) was significantly upregulated after paclitaxel injection. Inhibition of AKAP150 via siRNA or AKAP150(flox/flox) in rodents alleviated the pain behavior induced by paclitaxel, and partly restored the decreased calcineurin (CN) phosphatase activity after paclitaxel treatment. Paclitaxel decreased the expression of anti-inflammatory cytokine interleukin-4 (IL-4), and intrathecal injections of IL-4 effectively alleviated paclitaxel-induced hypersensitivity and the frequency of dorsal root ganglion (DRG) neurons action potential. The decreased CN enzyme activity...
Source: Brain, Behavior, and Immunity - October 19, 2017 Category: Neurology Authors: Nie B, Liu C, Bai X, Chen X, Wu S, Zhang S, Huang Z, Xie M, Xu T, Xin W, Zeng W, Ouyang H Tags: Brain Behav Immun Source Type: research

Long Noncoding RNA H19 Promotes Neuroinflammation in Ischemic Stroke by Driving Histone Deacetylase 1-Dependent M1 Microglial Polarization Basic Sciences
Conclusions—Our findings indicate that H19 promotes neuroinflammation by driving HDAC1-dependent M1 microglial polarization, suggesting a novel H19-based diagnosis and therapy for ischemic stroke.
Source: Stroke - July 24, 2017 Category: Neurology Authors: Jue Wang, Haiping Zhao, Zhibin Fan, Guangwen Li, Qingfeng Ma, Zhen Tao, Rongliang Wang, Juan Feng, Yumin Luo Tags: Animal Models of Human Disease, Cerebrovascular Disease/Stroke, Ischemic Stroke Original Contributions Source Type: research

TRAF6 participates in early brain injury after subarachnoid hemorrhage in rats through inhibiting autophagy and promoting oxidative stress
This study was designed to explore changes of expression level and potential roles and mechanisms of TRAF6 in early brain injury (EBI) after SAH by using a Sprague–Dawley rat model of SAH induced in 0.3 ml non‐heparinized autologous arterial blood injected into the prechiasmatic cistern. First, compared with the sham group, we found that the expression levels of TRAF6 increased gradually and peaked at 24 h after SAH. Second, the results showed that application of TRAF6 overexpression plasmid and genetic silencing siRNA could increase or decrease expression of TRAF6, respectively, and severely exacerbate or relieve EBI ...
Source: Journal of Neurochemistry - May 24, 2017 Category: Neurology Authors: Yang Dou, Haitao Shen, Dongxia Feng, Haiying Li, Xiaodi Tian, Jian Zhang, Zhong Wang, Gang Chen Tags: Original Article Source Type: research

Role of PDGF-D and PDGFR-β in neuroinflammation in experimental ICH mice model.
CONCLUSION: ICH-induced PDGF-D accumulation contributed to post-ICH inflammation via PDGFR activation and enhanced macrophage infiltration. The inhibition of PDGFR had an anti-inflammatory effect. Plasmin is a possible upstream effector of PDGF-D. The targeting of PDGF-D may provide a novel way to decrease brain injury after ICH. PMID: 27302678 [PubMed - as supplied by publisher]
Source: Experimental Neurology - June 10, 2016 Category: Neurology Authors: Yang P, Manaenko A, Xu F, Miao L, Wang G, Hu X, Guo ZN, Hu Q, Hartman RE, Pearce WJ, Obenaus A, Zhang JH, Chen G, Tang J Tags: Exp Neurol Source Type: research

Gypenoside Attenuates β Amyloid-Induced Inflammation in N9 Microglial Cells via SOCS1 Signaling.
In this study, we hypothesized that GP attenuates Aβ-induced microglial activation by ameliorating microglial M1/M2 states, and the process may be mediated by suppressor of cell signaling protein 1 (SOCS1). In this study, we found that Aβ exposure increased the levels of microglial M1 markers, including iNOS expression, tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and IL-6 releases, and coadministration of GP reversed the increase of M1 markers and enhanced the levels of M2 markers, including arginase-1 (Arg-1) expression, IL-10, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophi...
Source: Neural Plasticity - May 25, 2016 Category: Neurology Authors: Cai H, Liang Q, Ge G Tags: Neural Plast Source Type: research

JNK Activation Contributes to Oxidative Stress-Induced Parthanatos in Glioma Cells via Increase of Intracellular ROS Production
In this study, we used glioma cell lines and H2O2 to investigate the role of JNK in glioma cell parthanatos induced by oxidative stress. We found that exposure to H2O2 not only induced intracellular accumulation of ROS but also resulted in glioma cell death in a concentration- and incubation time-dependent manner, which was accompanied with cytoplasmic formation of PAR polymer, expressional upregulation of PARP-1, mitochondrial depolarization, and AIF translocation to nucleus. Pharmacological inhibition of PARP-1 with 3AB or genetic knockdown of its level with siRNA rescued glioma cell death, as well as suppressed cytoplas...
Source: Molecular Neurobiology - May 15, 2016 Category: Neurology Source Type: research

Clinacanthus nutans Protects Cortical Neurons Against Hypoxia-Induced Toxicity by Downregulating HDAC1/6
This study further opens a new avenue for the use of herbal medicines to regulate epigenetic control of brain injury.
Source: NeuroMolecular Medicine - May 9, 2016 Category: Neurology Source Type: research

Strategies to target drugs to gliomas and CNS metastases of solid tumors
Abstract The treatment for central nervous system metastases of solid tumors and gliomas is limited as the blood–brain barrier (BBB) is an obstacle to systemic therapy. Here, we review the physiochemical properties of the BBB and both current and new drug strategies to penetrate brain tumors. We focus on targeting receptor- or carrier-mediated transport mechanisms over the BBB used by drug conjugates, nanoparticles, polymer-based nanocarriers, siRNA, and antibodies.
Source: Journal of Neurology - October 17, 2015 Category: Neurology Source Type: research

Silencing of Id2 attenuates hypoxia/ischemia-induced neuronal injury via inhibition of neuronal apoptosis.
This study was aimed to investigate whether knockdown of Id2 in neuronal cells could protect them from hypoxic and ischemic injury both in vitro and in vivo. Flow cytometric analysis was employed to assess neuronal apoptosis in CoCl2-treated neuroblastoma B35 cells engineered to overexpress or knockdown Id2 expression. In vivo knockdown of Id2 was performed in Sprague-Dawley rats by a single intracerebroventricular injection of Cy3-labeled and cholesterol-modified Id2-siRNA. We found that knockdown of Id2 attenuated H/I-induced neuronal apoptosis in vitro while overexpression of Id2 produced an opposite effect. In a rat mo...
Source: Behavioural Brain Research - July 14, 2015 Category: Neurology Authors: Guo L, Yang X, Lin X, Lin Y, Shen L, Nie Q, Ren L, Guo Q, Que S, Qiu Y Tags: Behav Brain Res Source Type: research

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