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Source: Journal of Neurochemistry
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Total 123 results found since Jan 2013.
Emerging role of PARP ‐1 and PARthanatos in ischemic stroke
AbstractCell death is a key feature of neurological diseases, including stroke and neurodegenerative disorders. Studies in a variety of ischemic/hypoxic mouse models demonstrate that poly(ADP-ribose) polymerase-1 (PARP-1)-dependent cell death, also named PARthanatos, plays a pivotal role in ischemic neuronal cell death and disease progress. PARthanatos has its unique triggers, processors, and executors that convey a highly orchestrated and programmed signaling cascade. In addition to its role in gene transcription, DNA damage repair, and energy homeostasis through PARylation of its various targets, PARP-1 activation in neu...
Source: Journal of Neurochemistry - July 9, 2021 Category: Neuroscience Authors: Shuiqiao Liu,
Weibo Luo,
Yingfei Wang Tags: REVIEW Source Type: research
Ganglioside GD3 is Up ‐regulated in Microglia and Regulates Phagocytosis Following Global Cerebral Ischemia
ABSTRACTGangliosides, the major sialic-acid containing glycosphingolipids in the mammalian brain, play important roles in brain development and neural functions. Here, we show that the b-series ganglioside GD3 and its biosynthetic enzyme, GD3-synthase (GD3S), were up-regulated predominantly in the microglia of mouse hippocampus from 2 to 7 days following global cerebral ischemia (GCI). Interestingly, GD3S knockout (GD3S-KO) mice exhibited decreased hippocampal neuronal loss following GCI, as compared to wild-type (WT) mice. While comparable levels of astrogliosis and microglial proliferation were observed between WT and GD...
Source: Journal of Neurochemistry - June 16, 2021 Category: Neuroscience Authors: Jing Wang,
Quanguang Zhang,
Yujiao Lu,
Yan Dong,
Krishnan M. Dhandapani,
Darrell W. Brann,
Robert K Yu Tags: ORIGINAL ARTICLE Source Type: research
Is there a role for the p75 neurotrophin receptor in mediating degeneration during oxidative stress and after hypoxia?
AbstractCholinergic basal forebrain (cBF) neurons are particularly vulnerable to degeneration following trauma and in neurodegenerative conditions. One reason for this is their characteristic expression of the p75 neurotrophin receptor (p75NTR), which is upregulated and mediates neuronal death in a range of neurological and neurodegenerative conditions, including dementia, stroke, and ischaemia. The signalling pathway by which p75NTR signals cell death is incompletely characterised, but typically involves activation by neurotrophic ligands and signalling through c-jun kinase, resulting in caspase activation via mitochondri...
Source: Journal of Neurochemistry - June 10, 2021 Category: Neuroscience Authors: Kornraviya Sankorrakul,
Lei Qian,
Wipawan Thangnipon,
Elizabeth J Coulson Tags: REVIEW Source Type: research
Activation of neuronal Ras ‐related C3 botulinum toxin substrate 1 (Rac1) improves post‐stroke recovery and axonal plasticity in mice
We propose that activation of neuronal Rac1 mediates the release of BDNF via PAK1 signaling, which further promotes axonal plasticity and alleviates astrogliosis, and eventually contributes to functional recovery after brain ischemia. Targeting neuronal Rac1 may offer a potential therapeutic target for promoting brain remapping and functional recovery after stroke. AbstractLong-term disability after stroke is common but the mechanisms of post-stroke recovery remain unclear. Cerebral Ras-related C3 botulinum toxin substrate (Rac) 1 contributes to functional recovery after ischemic stroke in mice. As Rac1 plays divergent rol...
Source: Journal of Neurochemistry - May 22, 2021 Category: Neuroscience Authors: Fan Bu,
Yashasvee Munshi,
J Weldon Furr,
Jia ‐wei Min,
Li Qi,
Anthony Patrizz,
Zachary R. Spahr,
Akihiko Urayama,
Julia K. Kofler,
Louise D. McCullough,
Jun Li Tags: ORIGINAL ARTICLE Source Type: research
Single intracerebroventricular progranulin injection adversely affects the blood –brain barrier in experimental traumatic brain injury
In conclusion, single ICV administr ation of rPGRN had not the expected protective effects in the acute phase of murine TBI, but appeared to cause an aggravation of blood–brain barrier disruption. The data raise questions about putative PGRN‐boosting approaches in other types of brain injuries and disease.
Source: Journal of Neurochemistry - May 13, 2021 Category: Neuroscience Authors: Regina Hummel,
Manuel Lang,
Simona Walderbach,
Yong Wang,
Irmgard Tegeder,
Christina G ölz,
Michael K. E. Schäfer Tags: ORIGINAL ARTICLE Source Type: research
Single intracerebroventricular progranulin injection adversely affects the blood ‐brain barrier in experimental traumatic brain injury
In conclusion, single ICV administration of rPGRN had not the expected protective effects in the acute phase of murine TBI, but appeared to cause an aggravation of blood‐brain barrier disruption. The data raise questions about putative PGRN‐boosting approaches in other types of brain injuries and disease.
Source: Journal of Neurochemistry - April 26, 2021 Category: Neuroscience Authors: Regina Hummel,
Manuel Lang,
Simona Walderbach,
Yong Wang,
Irmgard Tegeder,
Christina G ölz,
Michael K.E. Schäfer Tags: ORIGINAL ARTICLE Source Type: research
Acute motor deficit and subsequent remyelination ‐associated recovery following internal capsule demyelination in mice
In this issue, we examined the effect of focal internal capsule (IC) demyelination on motor behavior in mice. We found that lysophosphatidylcholine (LPC) induced demyelination at the IC resulted in acute asymmetric motor deficit, followed by subsequent remyelination ‐associated functional recovery. Our results suggest that IC demyelination is a tractable model for characterizing demyelination and remyelination through behavioral measurements, and may be used to complement future drug discovery efforts for promoting repair in inflammatory demyelinating disorde rs, such as multiple sclerosis (MS). Images generated with Bio...
Source: Journal of Neurochemistry - April 2, 2021 Category: Neuroscience Authors: Reiji Yamazaki,
Nobuhiko Ohno,
Jeffrey K. Huang Tags: Original Article Source Type: research
Issue Cover (March 2021)
Front cover:Necrostatin ‐1 (Nec‐1) has been shown to inhibit necroptosis. The mitochondrial protein Bcl‐2/adenovirus E1B 19‐kDa interacting protein 3 (BNIP3) activates a type of caspase‐independent cell death that is similar to necroptosis. Here we show that Nec‐1 is protective against death of neurons and olig odendrocytes in traumatic brain injury (TBI) in mice and in ischemic stroke in rats by inhibiting BNIP3; Nec‐1 prevents BNIP3 from integration into mitochondria to block the BNIP3 cell death pathway. The data suggest that Nec‐1 is a novel inhibitor for BNIP3.Image Content: Nec‐1 preserves structur...
Source: Journal of Neurochemistry - April 2, 2021 Category: Neuroscience Tags: Issue Cover Source Type: research
Validation of Cerebral Blood Flow Connectivity as Imaging Prognostic Biomarker on Subcortical Stroke
AbstractStroke is a major cause of vascular cognitive dysfunction, such as memory impairment. We aimed to explore the neural substrates underlying verbal memory impairment in subcortical stroke patients by the methods of voxel ‐wise cerebral blood flow (CBF) and the functional covariance network (FCN). Sixty patients with chronic subcortical stroke and sixty normal controls (NCs) were recruited into this study. We used three‐dimensional pseudo‐continuous arterial spin‐labeling imaging to measure alterations in CBF and FCNs. We mapped the overall CBF alterations in a voxel‐wise manner and compared CBF measurements...
Source: Journal of Neurochemistry - March 29, 2021 Category: Neuroscience Authors: Caihong Wang,
Peifang Miao,
Jingchun Liu,
Zhen Li,
Ying Wei,
Yingying Wang,
Yong Zhang,
Kaiyu Wang,
Jingliang Cheng Tags: ORIGINAL ARTICLE Source Type: research
Ferroptosis: an emerging therapeutic target in stroke
AbstractStroke is a disastrous neurological disease with high morbidity and mortality. The mechanism of the pathological process is extremely complicated and unclear. Although many basic studies have confirmed some molecular mechanism of brain injury after stroke, these studies cannot effectively translate into treatment and clinical application. Ferroptosis is a form of cell death that is distinct from necrosis, apoptosis, and autophagy morphologically and biochemically, and is characterized by iron‐dependent accumulation of lipid peroxides. Despite ferroptosis being first identified in cancer cells, it was recently ...
Source: Journal of Neurochemistry - March 18, 2021 Category: Neuroscience Authors: Yibo Liu,
Yuanjian Fang,
Zeyu Zhang,
Yujie Luo,
Anke Zhang,
Cameron Lenahan,
Sheng Chen Tags: REVIEW ARTICLE Source Type: research
AMPK ‐regulated miRNA‐210‐3p is activated during ischaemic neuronal injury and modulates PI3K‐p70S6K signalling
We report a robust induction of microRNA miR‐210‐3p bothin vitro in primary cortical neurons in response to acute AMPK activation and following ischaemic strokein vivo. Bioinformatics and reverse phase protein array analysis of neuronal protein expression changesin vivo following administration of a miR ‐210‐3p mimic revealed altered expression of phosphatase and tensin homolog (PTEN), 3‐phosphoinositide‐dependent protein kinase 1 (PDK1), ribosomal protein S6 kinase (p70S6K) and ribosomal protein S6 (RPS6) signalling in response to increasing miR‐210‐3p.In vivo, we observed a corresponding reduction in p70S...
Source: Journal of Neurochemistry - March 11, 2021 Category: Neuroscience Authors: Shona Pfeiffer,
Anna Toma šcová,
Uta Mamrak,
Stefan J. Haunsberger,
Niamh M.C. Connolly,
Alexa Resler,
Heiko Düssmann,
Petronela Weisová,
Elisabeth Jirström,
Beatrice D’Orsi,
Gang Chen,
Mattia Cremona,
Bryan T. Hennessy,
Nikolaus Plesn Tags: ORIGINAL ARTICLE Source Type: research
PSD ‐93 mediates the crosstalk between neuron and microglia and facilitates acute ischemic stroke injury by binding to CX3CL1
In this study, we examined the interaction of PSD‐93 and CX3CL1 in the crosstalk between neurons and microglia in acute ischemic stroke. We utiliz ed male C57BL/6 mice to establish the middle cerebral artery occlusion model (MCAO) and designed a fusion small peptide Tat‐CX3CL1 (357‐395aa) to inhibit PSD‐93 and CX3CL1 interaction. The combination peaks of PSD‐93 and CX3CL1 at 6 hr after I/R were observed. The binding sites were located at the 420–535 amino acid sequence of PSD‐93 and 357–395 amino acid sequence of CX3CL1. Tat‐CX3CL1 (357‐395aa) could inhibit the interaction of PSD‐93 and CX3CL1 and in...
Source: Journal of Neurochemistry - March 8, 2021 Category: Neuroscience Authors: Qingxiu Zhang,
Lei He,
Mo Chen,
Hui Yang,
Xiaowei Cao,
Xiaomei Liu,
Qi Hao,
Zhengwei Chen,
Tengfei Liu,
Xiu ‐e Wei,
Liangqun Rong Tags: ORIGINAL ARTICLE Source Type: research
Regulators of cholinergic signaling in disorders of the central nervous system
AbstractCholinergic signaling is crucial in cognitive processes and degenerating cholinergic projections are a pathological hallmark in dementia. Use of cholinesterase inhibitors is currently the main treatment option to alleviate symptoms of Alzheimer ’s disease and has been postulated as a therapeutic strategy in acute brain damage (stroke, traumatic brain injury). However, the benefits of this treatment are still not clear. Importantly, cholinergic receptors are expressed both by neurons and by astrocytes and microglia, and binding of acetylc holine to the α7 nicotinic receptor in glial cells results in anti‐inflam...
Source: Journal of Neurochemistry - February 27, 2021 Category: Neuroscience Authors: Katarzyna Winek,
Hermona Soreq,
Andreas Meisel Tags: REVIEW Source Type: research
PSD ‐93 mediates the crosstalk between neuron and microglia and facilitates acute ischemic stroke injury by binding to CX3CL1
In this study, we examined the interaction of PSD‐93 and CX3CL1 in the crosstalk between neuron and microglia in acute ischemic stroke. We utilized male C57BL/6 mice to establi sh middle cerebral artery occlusion model (MCAO) and designed a fusion small peptide Tat‐CX3CL1 (357‐395aa) to inhibit PSD‐93 and CX3CL1 interaction. The combination peaks of PSD‐93 and CX3CL1 at 6 h after I/R were observed. The binding sites were located at the 420‐535 amino acid sequence of PSD‐93 and 357‐395 amino acid sequence of CX3CL1. Tat‐CX3CL1 (357‐395aa) could inhibit the interaction of PSD‐93 and CX3CL1 and inhibited...
Source: Journal of Neurochemistry - February 18, 2021 Category: Neuroscience Authors: Qingxiu Zhang,
Lei He,
Mo Chen,
Hui Yang,
Xiaowei Cao,
Xiaomei Liu,
Qi Hao,
Zhengwei Chen,
Tengfei Liu,
Xiu ‐e Wei,
Liangqun Rong Tags: ORIGINAL ARTICLE Source Type: research
