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Source: Journal of Neurochemistry

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Total 59 results found since Jan 2013.

COUP ‐TFII plays a role in cAMP‐induced Schwann cell differentiation and in vitro myelination by upregulating Krox20
AbstractSchwann cells (SCs) are known to produce myelin for saltatory nerve conduction in the peripheral nervous system (PNS). SC differentiation and myelination processes are controlled by several transcription factors including Sox10, Oct6/Pou3f1, and Krox20/Egr2. Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII/NR2F2) is an orphan receptor that plays a role in the development and differentiation. However, the role of COUP-TFII in the transcriptional regulatory network of SC differentiation has not been fully identified yet. Thus, the objective of this study was to investigate the role and molecular...
Source: Journal of Neurochemistry - January 17, 2023 Category: Neuroscience Authors: Sang ‐Heum Han, Young Hee Kim, Su‐Jeong Park, Jun‐Gi Cho, Yoon Kyung Shin, Young Bin Hong, Jeanho Yun, Jin‐Yeong Han, Hwan Tae Park, Joo‐In Park Tags: ORIGINAL ARTICLE Source Type: research

Brain ‐derived neurotrophic factor (BDNF) induces antagonistic action to Nogo signaling by the upregulation of lateral olfactory tract usher substance (LOTUS) expression
This study examined molecular mechanism of regulation in LOTUS expression and found that brain-derived neurotrophic factor (BDNF) increased LOTUS expression in cultured hippocampal neurons. Exogenous application of BDNF increased LOTUS expression at both mRNA and protein levels in a dose-dependent manner. We also found that pharmacological inhibition with K252a and gene knockdown by siRNA of tropomyosin-related kinase B (TrkB), BDNF receptor suppressed BDNF-induced increase in LOTUS expression. Further pharmacological analysis of the TrkB signaling pathway revealed that BDNF increased LOTUS expression through mitogen-activ...
Source: Journal of Neurochemistry - November 30, 2022 Category: Neuroscience Authors: Junpei Matsubayashi, Yuki Kawaguchi, Yutaka Kawakami, Kohtaro Takei Tags: ORIGINAL ARTICLE Source Type: research

Centromere protein J is overexpressed in human glioblastoma and promotes cell proliferation and migration
AbstractGlioblastoma is the most common and malignant type of primary brain tumor. Previous studies have shown that alterations in centrosome amplification and its components are frequently found in treatment-resistant tumors and may be associated with tumor progression. A centrosome protein essential for centrosome biogenesis is the centromere protein J (CENPJ), known to control the proliferation of neural progenitors and hepatocarcinoma cells, and also neuronal migration. However, it remains unknown the role of CENPJ in glioblastoma. Here we show that CENPJ is overexpressed in human glioblastoma cell lines in comparison ...
Source: Journal of Neurochemistry - July 7, 2022 Category: Neuroscience Authors: Gabriella P. A. de Freitas, Luiz Henrique M. Geraldo, Bruna M. Faria, Soniza Vieira Alves ‐Leon, Jorge Marcondes de Souza, Vivaldo Moura‐Neto, Bruno Pontes, Luciana F. Romão, Patrícia P. Garcez Tags: ORIGINAL ARTICLE Source Type: research

Thioredoxin interacting protein drives astrocytic glucose hypometabolism in corticosterone ‐induced depressive state
In this study, we firstly applied18F-FDG PET and observed brain glucose hypometabolism in prefrontal cortex (PFC) of corticosterone-induced depression of rats. Next, astrocytic glucose hypometabolism was identified in PFC slices in in both corticosterone-induced depression of rats and cultured primary astrocytes from newborn rat PFC after stress-level corticosterone (100 nM) stimulation. Furthermore, we found the blockage of glucose uptake and the decrease of plasma membrane (PM) translocation of glucose transporter 1 (GLUT1) in astrocytic glucose hypometabolism under depressive condition. Interestingly, thioredoxin intera...
Source: Journal of Neurochemistry - August 9, 2021 Category: Neuroscience Authors: Shu ‐Man Pan, Ying Pan, Ya‐Li Tang, Na Zuo, Yan‐Xiu Zhang, Ke‐Ke Jia, Ling‐Dong Kong Tags: ORIGINAL ARTICLE Source Type: research

Fragile X mental retardation protein ‐regulated proinflammatory cytokine expression in the spinal cord contributes to the pathogenesis of inflammatory pain induced by complete Freund's adjuvant
AbstractStudies have verified that Fragile X mental retardation protein (FMRP), an RNA-binding protein, plays a potential role in the pathogenesis of formalin- and (RS)-3,5-dihydroxyphenylglycine (DHPG)-induced abnormal pain sensations. However, the role of FMRP in inflammatory pain has not been reported. Here, we showed an increase in FMRP expression in the spinal dorsal horn (SDH) in a rat model of inflammatory pain induced by complete Freund ’s adjuvant (CFA). Double immunofluorescence staining revealed that FMRP was mainly expressed in spinal neurons and colocalized with proinflammatory cytokines [tumor necrosis fact...
Source: Journal of Neurochemistry - August 2, 2021 Category: Neuroscience Authors: Yixin Yang, Jinsong Zhao, Yunze Li, Xiangyao Li, Xiaowei Chen, Zhiying Feng Tags: ORIGINAL ARTICLE Source Type: research

Spinal Nrf2 translocation may inhibit neuronal NF ‐κB activation and alleviate allodynia in a rat model of bone cancer pain
This study aimed to test the hypothesis that BCP induces the transfer of Nrf2 from the cytoplasm to the nucleus and further promotes nuclear transcription to activate heme oxygenase-1 (HO-1) and inhibit the activation of nuclear factor-kappa B (NF- κB) signalling, ultimately regulating the neuroinflammatory response. Von-Frey was used for behavioural analysis in BCP rats, while western blotting, real-time quantitative PCR (RT-PCR), and enzyme-linked immunosorbent assay (ELISA) were used to detect molecular expression changes, and immunofluore scence was used to detect cellular localization. We demonstrated that BCP induce...
Source: Journal of Neurochemistry - July 14, 2021 Category: Neuroscience Authors: Jie Fu, Chaobo Ni, Hua ‐Dong Ni, Long‐Sheng Xu, Qiu‐Li He, Huan Pan, Dong‐Dong Huang, Yan‐Bao Sun, Ge Luo, Ming‐Juan Liu, Ming Yao Tags: ORIGINAL ARTICLE Source Type: research

Targeting transthyretin ‐ Mechanism‐based treatment approaches and future perspectives in hereditary amyloidosis
Transthyretin (TTR) is a tetrameric transport protein that causes amyloid formation if destabilized. ATTR ‐amyloidosis is a progressive systemic disease with polyneuropathy and cardiomyopathy as the most abundant manifestations. Approved treatment approaches comprise sequence‐specific mRNA degradation and tetramer stabilization. Ongoing clinical trials assess the potential of GalNAc formulations to improve the administration of small interfering RNA and antisense oligonucleotides. A future TTR‐stabilizer with the potential to cross the blood‐brain barrier is tolcapone. Amyloid‐directed antibodies aim at reducing ...
Source: Journal of Neurochemistry - April 2, 2021 Category: Neuroscience Authors: Maike F. Dohrn, Sandra Ihne, Ute Hegenbart, Jessica Medina, Stephan L. Z üchner, Teresa Coelho, Katrin Hahn Tags: Review Article Source Type: research

Targeting transthyretin – mechanism‐based treatment approaches and future perspectives in hereditary amyloidosis
AbstractThe liver ‐derived, circulating transport protein transthyretin (TTR) is the cause of systemic hereditary (ATTRv) and wildtype (ATTRwt) amyloidosis. TTR stabilization and knockdown are approved therapies to mitigate the otherwise lethal disease course. To date, the variety in phenotypic penetrance and organ tropism is not fully understood. This systematic review summarizes the current literature on TTR pathophysiology with its therapeutic implications. Tetramer dissociation is the rate‐limiting step of amyloidogenesis. Besides destabilizingTTR mutations, other genetic (RBP4,APCS, AR, ATX2, C1q, C3) and external...
Source: Journal of Neurochemistry - November 6, 2020 Category: Neuroscience Authors: Maike F. Dohrn, Sandra Ihne, Ute Hegenbart, Jessica Medina, Stephan Z üchner, Teresa Coelho, Katrin Hahn Tags: REVIEW Source Type: research

Glycogen synthase kinase ‐3ß supports serotonin transporter function and trafficking in a phosphorylation‐dependent manner
AbstractSerotonin (5 ‐HT) transporter (SERT) plays a crucial role in serotonergic transmission in the central nervous system, and any aberration causes serious mental illnesses. Nevertheless, the cellular mechanisms that regulate SERT function and trafficking are not entirely understood. Growing evidence suggests that several protein kinases act as modulators. Here we delineate the molecular mechanisms by which glycogen synthase kinase‐3ß (GSK3ß) regulates SERT. When mouse striatal synaptosomes were treated with the GSK3α/ß inhibitor CHIR99021, we observed a significant increase in SERT function, Vmax, surface expr...
Source: Journal of Neurochemistry - August 13, 2020 Category: Neuroscience Authors: Ragu Varman Durairaj, Lankupalle D. Jayanthi, Sammanda Ramamoorthy Tags: ORIGINAL ARTICLE Source Type: research

Epigenetic Restoration of Voltage ‐gated Potassium Channel Kv1.2 Alleviates Nerve Injury‐induced Neuropathic Pain
AbstractVoltage ‐gated potassium channels (Kv) are important regulators of neuronal excitability for its role of regulating resting membrane potential and repolarization. Recent studies show that Kv channels participate in neuropathic pain, but the detailed underlying mechanisms are far from being clear. In the c urrent study, we used siRNA, miR‐137 agomir and antagomir to regulate the expression of Kv1.2 in spinal cord and dorsal root ganglia (DRG) of naïve and chronic constriction injury (CCI) rats. Kv currents and neuron excitability in DRG neurons were examined by patch‐clamp whole‐cell recording to verify the...
Source: Journal of Neurochemistry - July 2, 2020 Category: Neuroscience Authors: Jingjing Zhang, Lina Rong, Jinping Shao, Yidan Zhang, Yaping Liu, Sen Zhao, Lei Li, Wenli Yu, Mengya Zhang, Xiuhua Ren, Qingzan Zhao, Changlian Zhu, Huan Luo, Weidong Zang, Jing Cao Tags: ORIGINAL ARTICLE Source Type: research

Intermittent fasting promotes adult hippocampal neuronal differentiation by activating GSK ‐3β in 3xTg‐AD mice
AbstractModerate dietary restriction can ameliorate age ‐related chronic diseases such as Alzheimer's disease (AD) by increasing the expression of neurotrophic factors and promoting neurogenesis in the brain. Glycogen synthase kinase‐3β (GSK‐3β) signaling is essential for the coordination of progenitor cell proliferation and differentiation durin g brain development. The mechanisms by which GSK‐3β is involved in dietary restriction induced neurogenesis and cognitive improvement remain unclear. Six‐month‐old male 3xTg‐AD and wild type mice were fed on alternate days (intermittent fasting, IF) or ad libitum ...
Source: Journal of Neurochemistry - June 22, 2020 Category: Neuroscience Authors: Wei Li, Meijian Wu, Yilin Zhang, Xuemin Wei, Jiankun Zang, Yinghua Liu, Yanping Wang, Cheng ‐Xin Gong, Wei Wei Tags: ORIGINAL ARTICLE Source Type: research

H63D variant of the homeostatic iron regulator (HFE) gene alters α‐synuclein expression, aggregation, and toxicity
AbstractPathological features of Parkinson ’s disease include the formation of Lewy bodies containing α‐synuclein and the accumulation of iron in the substantia nigra. Previous studies have suggested that iron accumulation contributes to the Parkinson’s disease pathology through reactive oxygen species production and accelerated α‐ synuclein aggregation. The current study examines the effects of commonly occurring H63D variant of the homeostatic iron regulatory (HFE) gene on α‐synuclein pathology in cell culture and animal models. H63DHFE expression in SH ‐SY5Y cells lowered endogenous α‐synuclein levels ...
Source: Journal of Neurochemistry - June 22, 2020 Category: Neuroscience Authors: Yunsung Kim, Mark C. Stahl, Xuemei Huang, James R. Connor Tags: ORIGINAL ARTICLE Source Type: research

Occludin degradation makes brain microvascular endothelial cells more vulnerable to reperfusion injury in vitro
AbstractIntracerebral hemorrhage is the most dangerous complication in tPA thrombolytic therapy for ischemic stroke, which occurs as a consequence of endothelial cell death at the blood brain barrier (BBB) during thrombolytic reperfusion. We have previously shown that cerebral ischemia induced rapid occludin degradation and BBB disruption. Here we demonstrated an important role of occludin degradation in facilitating the evolution of ischemic endothelial cells towards death. Cultured brain microvascular endothelial cells (bEnd.3 cells) were exposed to oxygen ‐glucose deprivation (OGD) or incubated with occludin siRNA or ...
Source: Journal of Neurochemistry - June 11, 2020 Category: Neuroscience Authors: Yuan Zhang, Xiaofeng Li, Shanshan Qiao, Dexin Yang, Zongyang Li, Ji Xu, Weiping Li, Li Su, Wenlan Liu Tags: ORIGINAL ARTICLE Source Type: research

MicroRNA ‐22‐3p alleviates spinal cord ischemia/reperfusion injury by modulating M2 macrophage polarization via IRF5
AbstractCell death after spinal cord ischemia/reperfusion (I/R) can occur through necrosis, apoptosis and autophagy, resulting in changes to the immune environment. However, the molecular mechanism of this immune regulation is not clear. Accumulating evidence indicates that microRNAs (miRs) play a crucial role in the pathogenesis of spinal cord I/R injury. Here, we hypothesized miR ‐22‐3p may be involved in spinal cord I/R injury by interacting with interferon regulatory factor (IRF) 5. Rat models of spinal cord I/R injury were established by 12‐min occlusion of the aortic arch followed by 48‐h reperfusion, with L4...
Source: Journal of Neurochemistry - May 13, 2020 Category: Neuroscience Authors: Hua Fang, Miao Yang, Qin Pan, Hon ‐Ling Jin, Hua‐Feng Li, Ru‐Rong Wang, Quan‐Yun Wang, Jian‐Ping Zhang Tags: ORIGINAL ARTICLE Source Type: research