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Canonical pathways in stroke

Olivier Martinaud, Nicolas Mirlink, Sandrine Bioux, Evangéline Bliaux, Cécile Champmartin, Dorothée Pouliquen, Yohann Cruypeninck, Didier Hannequin, Emmanuel Gérardin
Agnosia for mirrored stimuli is a rare clinical deficit. Only eight patients have been reported in the literature so far and little is known about the neural substrates of this agnosia. Using a previously developed experimental test designed to assess this agnosia, namely the Mirror and Orientation Agnosia Test (MOAT), as well as voxel-lesion symptom mapping (VLSM), we tested the hypothesis that focal brain-injured patients with right parietal damage would be impaired in the discrimination between the canonical view of a visual object and its mirrored and rotated images...
May 2016: Cortex; a Journal Devoted to the Study of the Nervous System and Behavior
Antonio Berretta, Emma K Gowing, Christine L Jasoni, Andrew N Clarkson
Although recovery following a stroke is limited, undamaged neurons under the right conditions can establish new connections and take on-board lost functions. Sonic hedgehog (Shh) signaling is integral for developmental axon growth, but its role after injury has not been fully examined. To investigate the effects of Shh on neuronal sprouting after injury, we used an in vitro model of glial scar, whereby cortical astrocytes were mechanically traumatized to mimic reactive astrogliosis observed after stroke. This mechanical trauma impaired neurite outgrowth from post-natal cortical neurons plated on top of reactive astrocytes...
2016: Scientific Reports
Jie Yu, Zhuyun Jiang, Ling Ning, Zhilong Zhao, Na Yang, Lu Chen, Hui Ma, Li Li, Ya Fu, Huifeng Zhu, Hongyi Qi
Heat-shock protein 70 (HSP70) is known to function as a protective molecular chaperone that is massively induced in response to misfolded proteins following cerebral ischemia. The objective of this study was to characterize HSP70 induction by Z-ligustilide and explore its potential role in protection against cerebral ischemia-reperfusion injury. Our results demonstrated that the intranasal administration of Z-ligustilide reduced infarct volume and improved neurological function in a rat stroke model. Meanwhile, Z-ligustilide enhanced the cell viability of PC12 cells insulted by oxygen-glucose deprivation-reoxygenation (OGD-Reoxy) and decreased apoptotic and necrotic cell death...
2015: Biological & Pharmaceutical Bulletin
J M Calandria, A Asatryan, V Balaszczuk, E J Knott, B K Jun, P K Mukherjee, L Belayev, N G Bazan
Neuroprotectin D1 (NPD1), a docosahexaenoic acid (DHA)-derived mediator, induces cell survival in uncompensated oxidative stress (OS), neurodegenerations or ischemic stroke. The molecular principles underlying this protection remain unresolved. We report here that, in retinal pigment epithelial cells, NPD1 induces nuclear translocation and cREL synthesis that, in turn, mediates BIRC3 transcription. NPD1 activates NF-κB by an alternate route to canonical signaling, so the opposing effects of TNFR1 and NPD1 on BIRC3 expression are not due to interaction/s between NF-κB pathways...
August 2015: Cell Death and Differentiation
Li Wu, Yongjun Jiang, Juehua Zhu, Zhuoyu Wen, Xiaohui Xu, Xiaomeng Xu, Yi Xie, Lian Yang, Lili Xu, Wenya Lan, Gelin Xu, Xinfeng Liu
Vascular endothelial growth factor (VEGF) is a promising candidate for the treatment of ischemic stroke. However, accumulating evidence demonstrated that VEGF could exacerbate blood-brain barrier (BBB) disruption after ischemic stroke. This study was designed to investigate the underlying mechanisms. In the present study, a transient (90 min) middle cerebral artery occlusion (MCAO) model was performed to induce ischemic stroke in mice. VEGF was administered intracerebroventricularly 3h after reperfusion. A gene expression microarray was utilized to investigate the differentially expressed genes among the sham, MCAO, and VEGF groups...
October 2014: Brain Research Bulletin
Laurent O Mosnier, Berislav V Zlokovic, John H Griffin
Despite years of research and efforts to translate stroke research to clinical therapy, ischaemic stroke remains a major cause of death, disability, and diminished quality of life. Primary and secondary preventive measures combined with improved quality of care have made significant progress. However, no novel drug for ischaemic stroke therapy has been approved in the past decade. Numerous studies have shown beneficial effects of activated protein C (APC) in rodent stroke models. In addition to its natural anticoagulant functions, APC conveys multiple direct cytoprotective effects on many different cell types that involve multiple receptors including protease activated receptor (PAR) 1, PAR3, and the endothelial protein C receptor (EPCR)...
November 2014: Thrombosis and Haemostasis
Tao Huang, Dakuan Gao, Xiaofan Jiang, Shijie Hu, Lei Zhang, Zhou Fei
Resveratrol (Res) or trans-3,4',5-trihydroxystilbene, has been proven to exert neuroprotective effects in cerebral ischemia. The aim of the present study was to investigate whether Res has neuroprotective effects in primary cortical neurons subjected to transient oxygen-glucose deprivation (OGD) via inhibiting the expression of the gene encoding stromelysin-1, also known as matrix metalloproteinase-3 (MMP-3), and via inhibiting cell apoptosis. Primary cortical cells were exposed to OGD, followed by reoxygenation to induce transient ischemia...
August 2014: Molecular Medicine Reports
Xinyu Wang, James A Bynum, Solomon Stavchansky, Phillip D Bowman
Cellular damage from oxidative stress, in particular following ischemic injury, occurs during heart attack, stroke, or traumatic injury, and is potentially reducible with appropriate drug treatment. We previously reported that caffeic acid phenethyl ester (CAPE), a plant-derived polyphenolic compound, protected human umbilical vein endothelial cells (HUVEC) from menadione-induced oxidative stress and that this cytoprotective effect was correlated with the capacity to induce heme oxygenase-1 (HMOX1) and its protein product, a phase II cytoprotective enzyme...
July 5, 2014: European Journal of Pharmacology
Alexander R Edelmann, Sarah Schwartz-Baxter, Christopher F Dibble, Warren C Byrd, Jim Carlson, Ivandario Saldarriaga, Sompop Bencharit
UNLABELLED: Cerebral cavernous malformations (CCM) are vascular anomalies caused by mutations in genes encoding KRIT1, OSM and PDCD10 proteins causing hemorrhagic stroke. We examine proteomic change of loss of CCM gene expression. Using human umbilical vein endothelial cells, label-free differential protein expression analysis with multidimensional liquid chromatography/tandem mass spectrometry was applied to three CCM protein knockdown cell lines and two control cell lines: ProteomeXchange identifier PXD000362...
June 2014: Expert Review of Proteomics
Marco Francesco Morini, Elisabetta Dejana
PURPOSE OF REVIEW: The development of a functionally and anatomically correct vascular network is a complex phenomenon that requires the combined activity of different signaling pathways and transcription factors. Notch signaling activation, for instance, is crucial for arterial specification. Here, we discuss the current knowledge on how other signaling pathways cooperate with Notch to orchestrate arterial differentiation of embryonic and postnatal vasculature. RECENT FINDINGS: The role of Notch in vascular development and arterial differentiation is well known...
May 2014: Current Opinion in Hematology
Jaquette Liljencrantz, Andrew Marshall, Rochelle Ackerley, Håkan Olausson
Recently, several studies have suggested a role for unmyelinated (C-tactile, CT) low-threshold mechanoreceptive afferents in the allodynic condition. In this psychophysical study we explored the integrity of both Aβ and CT afferent processing following application of the heat capsaicin model of tactile allodynia on the left forearm in healthy subjects (n=40). We measured tactile direction discrimination (TDD) to target the integrity of Aβ processing (n=20). The TDD accuracy was significantly lower in the allodynic compared to a control zone...
March 20, 2014: Neuroscience Letters
Luis M Blanco-Colio
Cardiovascular diseases (CVD) are the first cause of mortality in Western countries. CVD include several pathologies such as coronary heart disease, stroke or cerebrovascular accident, congestive heart failure, peripheral arterial disease, and aortic aneurysm, among others. Interaction between members of the tumor necrosis factor (TNF) superfamily and their receptors elicits several biological actions that could participate in CVD. TNF-like weak inducer of apoptosis (TWEAK) and its functional receptor and fibroblast growth factor-inducible molecule 14 (Fn14) are two proteins belonging to the TNF superfamily that activate NF-κB by both canonical and non-canonical pathways and regulate several cell functions such as proliferation, migration, differentiation, cell death, inflammation, and angiogenesis...
2014: Frontiers in Immunology
Robert W Freilich, Maya E Woodbury, Tsuneya Ikezu
Neuroinflammation contributes to many neurologic disorders including Alzheimer's disease, multiple sclerosis, and stroke. Microglia is brain resident myeloid cells and have emerged as a key driver of the neuroinflammatory responses. MicroRNAs (miRNAs) provide a novel layer of gene regulation and play a critical role in regulating the inflammatory response of peripheral macrophages. However, little is known about the miRNA in inflammatory activation of microglia. To elucidate the role that miRNAs have on microglial phenotypes under classical (M1) or alternative (M2) activation under lipopolysaccharide ('M1'-skewing) and interleukin-4 ('M2a'-skewing) stimulation conditions, we performed microarray expression profiling and bioinformatics analysis of both mRNA and miRNA using primary cultured murine microglia...
2013: PloS One
François Binet, Gaëlle Mawambo, Nicholas Sitaras, Nicolas Tetreault, Eric Lapalme, Sandra Favret, Agustin Cerani, Dominique Leboeuf, Sophie Tremblay, Flavio Rezende, Aimee M Juan, Andreas Stahl, Jean-Sebastien Joyal, Eric Milot, Randal J Kaufman, Martin Guimond, Timothy E Kennedy, Przemyslaw Sapieha
In stroke and proliferative retinopathy, despite hypoxia driven angiogenesis, delayed revascularization of ischemic tissue aggravates the loss of neuronal function. What hinders vascular regrowth in the ischemic central nervous system remains largely unknown. Using the ischemic retina as a model of neurovascular interaction in the CNS, we provide evidence that the failure of reparative angiogenesis is temporally and spatially associated with endoplasmic reticulum (ER) stress. The canonical ER stress pathways of protein kinase RNA-like ER kinase (PERK) and inositol-requiring enzyme-1α (IRE1α) are activated within hypoxic/ischemic retinal ganglion neurons, initiating a cascade that results in angiostatic signals...
March 5, 2013: Cell Metabolism
Erin L Scott, Darrell W Brann
17β-estradiol (E2 or estrogen) is an endogenous steroid hormone that is well known to exert neuroprotection. Along these lines, one mechanism through which E2 protects the hippocampus from cerebral ischemia is by preventing the post-ischemic elevation of Dkk1, a neurodegenerative factor that serves as an antagonist of the canonical Wnt signaling pathway, and simultaneously inducing pro-survival Wnt/β-Catenin signaling in hippocampal neurons. Intriguingly, while expression of Dkk1 is required for proper neural development, overexpression of Dkk1 is characteristic of many neurodegenerative diseases, such as stroke, Alzheimer's disease, Parkinson's disease, and temporal lobe epilepsy...
June 13, 2013: Brain Research
Ji-An Pan, Yongjun Fan, Rajesh Kumar Gandhirajan, Muniswamy Madesh, Wei-Xing Zong
Intracellular calcium overload plays a critical role in numerous pathological syndromes such as heart failure, brain ischemia, and stroke. Hyperactivation of the acid-sensing ion channels including degenerin/epithelial amiloride-sensitive sodium (DEG/ENaC) channels has been shown to elevate intracellular calcium and cause subsequent neuronal cell death that is independent of the canonical Egl-1/Ced-9/Ced-4/Ced-3 apoptotic pathway in Caenorhabditis elegans. In mammalian cells, hyperactivation of the DEG/ENaC channels can also lead to cell death, although the underlying mechanism remains largely unknown...
February 1, 2013: Journal of Biological Chemistry
Yun Lin, Jian-Cheng Zhang, Jun Fu, Fang Chen, Jie Wang, Zhi-Lin Wu, Shi-Ying Yuan
Hyperforin, a lipophilic constituent of medicinal herb St John's wort, has been identified as the main active ingredient of St John's wort extract for antidepressant action by experimental and clinical studies. Hyperforin is currently known to activate transient receptor potential canonical (subtype) 6 (TRPC6) channel, increase the phosphorylated CREB (p-CREB), and has N-methyl-D-aspartate receptor-antagonistic effect that convert potential neuroprotective effects in vitro. However, the protective effects of hyperforin on ischemic stroke in vivo remain controversial and its neuroprotective mechanisms are still unclear...
February 2013: Journal of Cerebral Blood Flow and Metabolism
Mary F Lopez, David A Sarracino, Maryann Vogelsang, Jennifer N Sutton, Michael Athanas, Bryan Krastins, Alejandra Garces, Amol Prakash, Scott Peterman, Zareh Demirjian, Ignacio Inglessis-Azuaje, Kathleen Feeney, Mikaela Elia, David McMullin, G William Dec, Igor Palacios, Eng H Lo, Ferdinand Buonanno, MingMing Ning
Patent foramen ovale (PFO) is highly prevalent and associated with more than 150,000 strokes per year. Traditionally, it is thought that PFOs facilitate strokes by allowing venous clots to travel directly to the brain. However, only a small portion of PFO stroke patients have a known tendency to form blood clots, and the optimal treatment for this multiorgan disease is unclear. Therefore, mapping the changes in systemic circulation of PFO-related stroke is crucial in understanding the pathophysiology to individualize the best clinical treatment for each patient...
December 2012: Journal of Investigative Medicine: the Official Publication of the American Federation for Clinical Research
Mélanie Lalancette-Hébert, Vivek Swarup, Jean Martin Beaulieu, Ivan Bohacek, Essam Abdelhamid, Yuan Cheng Weng, Sachiko Sato, Jasna Kriz
Growing evidence suggests that galectin-3 is involved in fine tuning of the inflammatory responses at the periphery, however, its role in injured brain is far less clear. Our previous work demonstrated upregulation and coexpression of galectin-3 and IGF-1 in a subset of activated/proliferating microglial cells after stroke. Here, we tested the hypothesis that galectin-3 plays a pivotal role in mediating injury-induced microglial activation and proliferation. By using a galectin-3 knock-out mouse (Gal-3KO), we demonstrated that targeted disruption of the galectin-3 gene significantly alters microglia activation and induces ∼4-fold decrease in microglia proliferation...
July 25, 2012: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Edward T R Urban, Scott D Bury, H Scott Barbay, David J Guggenmos, Yafeng Dong, Randolph J Nudo
After cortical injury resulting from stroke, some recovery can occur and may involve spared areas of the cerebral cortex reorganizing to assume functions previously controlled by the damaged cortical areas. No studies have specifically assessed gene expression changes in remote neurons with axonal processes that terminate in the infarcted tissue, i.e., the subset of neurons most likely to be involved in regenerative processes. By physiologically identifying the primary motor area controlling forelimb function in adult rats (caudal forelimb area = CFA), and injecting a retrograde tract-tracer, we labeled neurons within the non-primary motor cortex (rostral forelimb area = RFA) that project to CFA...
October 2012: Molecular and Cellular Biochemistry
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