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Cx3cr1 stroke

Giulia Cisbani, Audrey Le Behot, Marie-Michèle Plante, Paul Préfontaine, Manon Lecordier, Serge Rivest
Stroke is the second cause of mortality worldwide and occurs following the interruption of cerebral blood circulation by cerebral vessel burst or subsequent to a local thrombus formation. Ischemic lesion triggers an important inflammatory response, characterized by massive infiltration of leukocytes, activation of glial cells and neurovascular reorganization. Chemokines and their receptors, such as CCR2 and CX3CR1, play an important role in leukocyte recruitment in the damaged area. Mice genetically depleted for the two receptors CCR2 and CX3CR1 underwent focal cerebral ischemia, based on the topical application of ferric chloride to truncate the distal middle cerebral artery...
March 12, 2018: Brain, Behavior, and Immunity
Jinkun Wang, Yan Gan, Pengcheng Han, Junxiang Yin, Qingwei Liu, Soha Ghanian, Feng Gao, Guanghui Gong, Zhiwei Tang
The chemokine fractalkine (CX3CL1) and its receptor CX3CR1 play a fundamental role in the pathophysiology of stroke. Previous studies have focused on a paracrine interaction between neurons that produce fractalkine and microglia that express CX3CR1 receptors in the central nervous system. Recent findings have demonstrated the functional expression of CX3CR1 receptors by hippocampal neurons, suggesting their involvement in neuroprotective and neurodegenerative actions. To elucidate the roles of neuronal CX3CR1 in neurodegeneration induced by ischemic stroke, a mouse model of permanent middle cerebral artery occlusion (pMCAO) was employed...
January 11, 2018: Scientific Reports
Benjamin Okyere, Miranda Creasey, Yeonwoo Lebovitz, Michelle H Theus
BACKGROUND: Leptomeningeal anastomoses play a critical role in regulating reperfusion following cerebrovascular obstruction; however, methods to evaluate their temporospatial remodeling remains under investigation. NEW METHOD: We combined arteriole-specific vessel painting with histological evaluation to assess the density and diameter of inter-collateral vessels between the middle cerebral artery and anterior cerebral artery (MCA-ACA) or posterior cerebral artery (MCA-PCA) in a murine model of permanent middle cerebral artery occlusion (pMCAO)...
January 1, 2018: Journal of Neuroscience Methods
Ruimin Ge, Daniel Tornero, Masao Hirota, Emanuela Monni, Cecilia Laterza, Olle Lindvall, Zaal Kokaia
BACKGROUND: Choroid plexus (CP) supports the entry of monocyte-derived macrophages (MDMs) to the central nervous system in animal models of traumatic brain injury, spinal cord injury, and Alzheimer's disease. Whether the CP is involved in the recruitment of MDMs to the injured brain after ischemic stroke is unknown. METHODS: Adult male C57BL/6 mice were subjected to focal cortical ischemia by permanent occlusion of the distal branch of the right middle cerebral artery...
July 28, 2017: Journal of Neuroinflammation
Yan-Zhi Liu, Chun Wang, Qian Wang, Yong-Zhong Lin, Yu-Song Ge, Dong-Mei Li, Geng-Sheng Mao
This study aims to explore the role of fractalkine/CX3C chemokine receptor 1 (CX3CR1) signaling pathway in the recovery of neurological functioning after an early ischemic stroke in rats. After establishment of permanent middle cerebral artery occlusion (pMCAO) models, 50 rats were divided into blank, sham, model, positive control and CX3CR1 inhibitor groups. Neurological impairment, walking and grip abilities, and cortical and hippocampal infarctions were evaluated by Zea Longa scoring criterion, beam-walking assay and grip strength test, and diffusion-weighted magnetic resonance imaging...
September 1, 2017: Life Sciences
Ulrika Wilhelmsson, Daniel Andersson, Yolanda de Pablo, Roy Pekny, Anders Ståhlberg, Jan Mulder, Nicholas Mitsios, Tibor Hortobágyi, Milos Pekny, Marcela Pekna
Microglia and astrocytes have been considered until now as cells with very distinct identities. Here, we assessed the heterogeneity within microglia/monocyte cell population in mouse hippocampus and determined their response to injury, by using single-cell gene expression profiling of cells isolated from uninjured and deafferented hippocampus. We found that in individual cells, microglial markers Cx3cr1, Aif1, Itgam, and Cd68 were co-expressed. Interestingly, injury led to the co-expression of the astrocyte marker Gfap in a subpopulation of Cx3cr1-expressing cells from both the injured and contralesional hippocampus...
June 1, 2017: Cerebral Cortex
Gerlinde van der Maten, Vivien Henck, Tadeusz Wieloch, Karsten Ruscher
BACKGROUND: The fractalkine/CX3 C chemokine receptor 1 (CX3 CR1) pathway has been identified to play an essential role in the chemotaxis of microglia, leukocyte trafficking and microglia/macrophage recruitment. It has also been shown to be important in the regulation of the inflammatory response in the early phase after experimental stroke. The present study was performed to investigate if CX3 CR1 deficiency affects microglia during the first 14 days with consequences for tissue damage after experimental stroke...
January 6, 2017: BMC Neuroscience
Yifang Fan, Xiaoxing Xiong, Yongming Zhang, Dongmei Yan, Zhihong Jian, Baohui Xu, Heng Zhao
BACKGROUND: MKEY, a synthetic cyclic peptide inhibitor of CXCL4-CCL5 heterodimer formation, has been shown to protect against atherosclerosis and aortic aneurysm formation by mediating inflammation, but whether it modulates neuroinflammation and brain injury has not been studied. We therefore studied the role of MKEY in stroke-induced brain injury in mice. METHODS AND RESULTS: MKEY was injected into mice after stroke with 60 minutes of middle cerebral artery occlusion...
September 15, 2016: Journal of the American Heart Association
Daojing Li, Chunjiong Wang, Yang Yao, Li Chen, Guiyou Liu, Rongxin Zhang, Qiang Liu, Fu-Dong Shi, Junwei Hao
Inflammatory factors secreted by microglia play an important role in focal ischemic stroke. The mammalian target of rapamycin (mTOR) pathway is a known regulator of immune responses, but the role that mTORC1 signaling plays in poststroke neuroinflammation is not clear. To explore the relationship between microglial action in the mTORC1 pathway and the impact on stroke, we administered the mTORC1 inhibitors sirolimus and everolimus to mice. Presumably, disrupting the mTORC1 pathway after focal ischemic stroke should clarify the subsequent activity of microglia...
October 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Rodney M Ritzel, Sarah J Pan, Rajkumar Verma, John Wizeman, Joshua Crapser, Anita R Patel, Richard Lieberman, Royce Mohan, Louise D McCullough
PURPOSE: The transient middle cerebral artery occlusion (MCAO) model of stroke is one of the most commonly used models to study focal cerebral ischemia. This procedure also results in the simultaneous occlusion of the ophthalmic artery that supplies the retina. Retinal cell death is seen days after reperfusion and leads to functional deficits; however, the mechanism responsible for this injury has not been investigated. Given that the eye may have a unique ocular immune response to an ischemic challenge, this study examined the inflammatory response to retinal ischemia in the MCAO model...
2016: Molecular Vision
Hyunjung Min, Yong Ho Jang, Ik-Hyun Cho, Seong-Woon Yu, Sung Joong Lee
BACKGROUND: Intracerebral hemorrhage (ICH) is one of the major causes of stroke. After onset of ICH, massive infiltration of macrophages is detected in the peri-hematoma regions. Still, the function of these macrophages in ICH has not been completely elucidated. RESULTS: In a collagenase-induced ICH model, CX3CR1(+) macrophages accumulated in the peri-hematoma region. Characterization of these macrophages revealed expression of alternatively activated (M2) macrophage markers...
April 19, 2016: Molecular Brain
Liang Wang, Shuai Kang, Dingquan Zou, Lei Zhan, Zhengxi Li, Wan Zhu, Hua Su
Ischemic stroke is a devastating complication of bone fracture. Bone fracture shortly after stroke enhances stroke injury by augmenting inflammation. We hypothesize that bone fracture shortly before ischemic stroke also exacerbates ischemic cerebral injury. Tibia fracture was performed 6 or 24 hours before permanent middle cerebral artery occlusion (pMCAO) on C57BL/6J mice or Ccr2RFP/+Cx3cr1GFP/+ mice that have the RFP gene knocked into one allele of Ccr2 gene and GFP gene knocked into one allele of Cx3cr1 gene...
2016: PloS One
David Fernández-López, Joel Faustino, Alexander L Klibanov, Nikita Derugin, Elodie Blanchard, Franziska Simon, Stephen L Leib, Zinaida S Vexler
Perinatal stroke leads to significant morbidity and long-term neurological and cognitive deficits. The pathophysiological mechanisms of brain damage depend on brain maturation at the time of stroke. To understand whether microglial cells limit injury after neonatal stroke by preserving neurovascular integrity, we subjected postnatal day 7 (P7) rats depleted of microglial cells, rats with inhibited microglial TGFbr2/ALK5 signaling, and corresponding controls, to transient middle cerebral artery occlusion (tMCAO)...
March 9, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Yanina R Timasheva, Timur R Nasibullin, Olga E Mustafina
Hypertension is the major risk factor for stroke, and genetic factors contribute to its development. Inflammation has been hypothesized to be the key link between blood pressure elevation and stroke. We performed an analysis of the association between inflammatory mediator gene polymorphisms and the incidence of stroke in patients with essential hypertension (EH). The study group consisted of 625 individuals (296 patients with noncomplicated EH, 71 hypertensive patients with ischemic stroke, and 258 control subjects)...
September 2015: Cerebrovascular Diseases Extra
Michael Gliem, Markus Schwaninger, Sebastian Jander
Hematogenous recruitment of monocytes and macrophages has traditionally been viewed as a harmful process causing exacerbation of brain injury after stroke. However, emerging findings suggest equally important protective features. Inflammatory monocytes are rapidly recruited to ischemic brain via a CCR2-dependent pathway and undergo secondary differentiation in the target tissue towards non-inflammatory macrophages, mediating neuroprotection and repair of the ischemic neurovascular unit. In contrast, independent recruitment of non-inflammatory monocytes via CX3CR1 does not occur...
March 2016: Biochimica et Biophysica Acta
Helene L Walter, Gerlinde van der Maten, Ana Rita Antunes, Tadeusz Wieloch, Karsten Ruscher
BACKGROUND: Recovery of lost neurological function after stroke is limited and dependent on multiple mechanisms including inflammatory processes. Selective pharmacological modulation of inflammation might be a promising approach to improve stroke outcome. METHODS: We used 1,1'-[1,4-phenylenebis(methylene)]bis[1,4,8,11-tetraazacyclotetradecane] (AMD3100), an antagonist to the C-X-C chemokine receptor type 4 (CXCR4) and potential allosteric agonist to CXCR7, administered to mice twice daily from day 2 after induction of photothrombosis (PT)...
2015: Journal of Neuroinflammation
Helene L Walter, Gerlinde van der Maten, Ana Rita Antunes, Tadeusz Wieloch, Karsten Ruscher
BACKGROUND: Recovery of lost neurological function after stroke is limited and dependent on multiple mechanisms including inflammatory processes. Selective pharmacological modulation of inflammation might be a promising approach to improve stroke outcome. METHODS: We used 1,1'-[1,4-phenylenebis(methylene)]bis[1,4,8,11-tetraazacyclotetradecane] (AMD3100), an antagonist to the C-X-C chemokine receptor type 4 (CXCR4) and potential allosteric agonist to CXCR7, administered to mice twice daily from day 2 after induction of photothrombosis (PT)...
December 2015: Journal of Neuroinflammation
Oana Herlea-Pana, Longbiao Yao, Janet Heuser-Baker, Qiongxin Wang, Qilong Wang, Constantin Georgescu, Ming-Hui Zou, Jana Barlic-Dicen
AIMS: Atherosclerosis manifests itself as arterial plaques, which lead to heart attacks or stroke. Treatments supporting plaque regression are therefore aggressively pursued. Studies conducted in models in which hypercholesterolaemia is reversible, such as the Reversa mouse model we have employed in the current studies, will be instrumental for the development of such interventions. Using this model, we have shown that advanced atherosclerosis regression occurs when lipid lowering is used in combination with bone-marrow endothelial progenitor cell (EPC) treatment...
May 1, 2015: Cardiovascular Research
Valérie Jolivel, Frank Bicker, Fabien Binamé, Robert Ploen, Stefanie Keller, René Gollan, Betty Jurek, Jérôme Birkenstock, Laura Poisa-Beiro, Julia Bruttger, Verena Opitz, Serge C Thal, Ari Waisman, Tobias Bäuerle, Michael K Schäfer, Frauke Zipp, Mirko H H Schmidt
The contribution of microglia to ischemic cortical stroke is of particular therapeutic interest because of the impact on the survival of brain tissue in the ischemic penumbra, a region that is potentially salvable upon a brain infarct. Whether or not tissue in the penumbra survives critically depends on blood flow and vessel perfusion. To study the role of microglia in cortical stroke and blood vessel stability, CX3CR1(+/GFP) mice were subjected to transient middle cerebral artery occlusion and then microglia were investigated using time-lapse two-photon microscopy in vivo...
February 2015: Acta Neuropathologica
Roslyn A Taylor, Matthew D Hammond, Youxi Ai, Lauren H Sansing
Intracerebral hemorrhage is a subset of stroke for which there is no specific treatment. The Ly6Chi CCR2+ monocytes have been shown to contribute to acute injury after intracerebral hemorrhage. The other murine monocyte subset expresses CX3CR1 and lower Ly6C levels, and contributes to repair in other disease models. We hypothesized that the Ly6Clo CX3CR1+ monocytes would contribute to recovery after intracerebral hemorrhage. Intracerebral hemorrhage was modeled by blood injection in WT and CX3CR1-null bone marrow chimeras...
2014: PloS One
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