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Canonical pathways in ischemic stroke

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
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
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
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
Zhi-Nian Lei, Fang Liu, Lin-Mei Zhang, Ya-Lin Huang, Feng-Yan Sun
Our previous experiments suggest that treatment with Bcl-2 increases proliferation and differentiation of neuronal progenitors induced by ischemic injury and ameliorates neurological functional deficits after stroke. However, in addition to its traditional anti-apoptotic effect, little is known about the concrete molecular modulation mechanism. In this study, Bcl-2-expressing plasmids were injected into the lateral ventricle of rat brains immediately following a 30-min occlusion of the middle cerebral artery to determine the role of Bcl-2 in adult neurogenesis...
July 2012: Neurochemistry International
Thomas Seifert-Held, Thomas Pekar, Thomas Gattringer, Nicole E Simmet, Hubert Scharnagl, Tatjana Stojakovic, Franz Fazekas, Maria K Storch
OBJECTIVES: Previous data suggest that Dickkopf-1 (Dkk-1), an inhibitor of the canonical/β-catenin cascade of the Wnt pathway, is upregulated in carotid atherosclerosis and acute myocardial ischemia. It is currently unclear if such upregulation also occurs in cerebral ischemia. METHODS: We measured plasma levels of Dkk-1 in patients with acute ischemic stroke (n=57) within 24h from symptom onset, in patients with clinically stable cerebrovascular disease (n=29) and in healthy controls (n=29)...
September 2011: Atherosclerosis
T L Barr, Y Conley, J Ding, A Dillman, S Warach, A Singleton, M Matarin
OBJECTIVE: The objective of this study was to provide insight into the molecular mechanisms of acute ischemic cerebrovascular syndrome (AICS) through gene expression profiling and pathway analysis. METHODS: Peripheral whole blood samples were collected from 39 MRI-diagnosed patients with AICS and 25 nonstroke control subjects ≥ 18 years of age. Total RNA was extracted from whole blood stabilized in Paxgene RNA tubes, amplified, and hybridized to Illumina HumanRef-8v2 bead chips...
September 14, 2010: Neurology
Wanlu Du, Junbo Huang, Hailan Yao, Kechun Zhou, Bo Duan, Yizheng Wang
Brain injury after focal cerebral ischemia, the most common cause of stroke, develops from a series of pathological processes, including excitotoxicity, inflammation, and apoptosis. While NMDA receptors have been implicated in excitotoxicity, attempts to prevent ischemic brain damage by blocking NMDA receptors have been disappointing. Disruption of neuroprotective pathways may be another avenue responsible for ischemic damage, and thus preservation of neuronal survival may be important for prevention of ischemic brain injury...
October 2010: Journal of Clinical Investigation
Federica Mastroiacovo, Carla L Busceti, Francesca Biagioni, Slavianka G Moyanova, Miriam H Meisler, Giuseppe Battaglia, Andrea Caricasole, Valeria Bruno, Ferdinando Nicoletti
Inhibition of the canonical Wnt pathway has been implicated in the pathophysiology of neuronal death. Here, we report that the secreted Wnt antagonist, Dickkopf-1 (Dkk-1) is rapidly induced in neurons after induction of focal brain ischemia. In rats undergoing transient focal ischemia in response to brain infusion of endothelin-1, Dkk-1 was induced in neurons of the ischemic core and the penumbra region. Induction of Dkk-1 was associated with a reduced expression of beta-catenin (a downstream signaling molecule of the canonical Wnt pathway), and was not observed in neurons expressing the protective protein, heat shock protein-70...
February 2009: Journal of Cerebral Blood Flow and Metabolism
Alexei Degterev, Zhihong Huang, Michael Boyce, Yaqiao Li, Prakash Jagtap, Noboru Mizushima, Gregory D Cuny, Timothy J Mitchison, Michael A Moskowitz, Junying Yuan
The mechanism of apoptosis has been extensively characterized over the past decade, but little is known about alternative forms of regulated cell death. Although stimulation of the Fas/TNFR receptor family triggers a canonical 'extrinsic' apoptosis pathway, we demonstrated that in the absence of intracellular apoptotic signaling it is capable of activating a common nonapoptotic death pathway, which we term necroptosis. We showed that necroptosis is characterized by necrotic cell death morphology and activation of autophagy...
July 2005: Nature Chemical Biology
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