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Macrophage stroke

M Asunción Barreda-Manso, Natalia Yanguas-Casás, Manuel Nieto-Sampedro, Lorenzo Romero-Ramírez
Following a central nervous system (CNS) injury, restoration of the blood-brain barrier (BBB) integrity is essential for recovering homeostasis. When this process is delayed or impeded, blood substances and cells enter the CNS parenchyma, initiating an additional inflammatory process that extends the initial injury and causes so-called secondary neuronal loss. Astrocytes and profibrotic mesenchymal cells react to the injury and migrate to the lesion site, creating a new glia limitans that restores the BBB. This process is beneficial for the resolution of the inflammation, neuronal survival and the initiation of the healing process...
October 18, 2016: Journal of Cellular Physiology
Ruihe Lin, Jingli Cai, Eric W Kostuk, Robert Rosenwasser, Lorraine Iacovitti
BACKGROUND: Dimethyl fumarate (DMF), working via its metabolite monomethylfumarate (MMF), acts as a potent antioxidant and immunomodulator in animal models of neurologic disease and in patients with multiple sclerosis. These properties and their translational potential led us to investigate whether DMF/MMF could also protect at-risk and/or dying neurons in models of ischemic stroke in vitro and in vivo. Although the antioxidant effects have been partially addressed, the benefits of DMF immunomodulation after ischemic stroke still need to be explored...
October 13, 2016: Journal of Neuroinflammation
Tao Yan, Poornima Venkat, Michael Chopp, Alex Zacharek, Ruizhuo Ning, Cynthia Roberts, Yi Zhang, Mei Lu, Jieli Chen
BACKGROUND AND PURPOSE: Comorbidity of diabetes mellitus and stroke results in worse functional outcome, poor long-term recovery, and extensive vascular damage. We investigated the neurorestorative effects and mechanisms of stroke treatment with human bone marrow-derived mesenchymal stromal cells (hMSCs) in type 2 diabetes mellitus (T2DM) rats. METHODS: Adult male Wistar rats were induced with T2DM, subjected to 2 hours of middle cerebral artery occlusion (MCAo) and treated via tail-vein injection with (1) PBS (n=8) and (2) hMSCs (n=10; 5×10(6)) at 3 days after MCAo...
October 11, 2016: Stroke; a Journal of Cerebral Circulation
Filip K Swirski, Matthias Nahrendorf, Peter Libby
Inflammation furnishes a series of pathogenic pathways that couple the risk factors for atherosclerosis with altered behavior of the intrinsic cells of the arterial wall, endothelium, and smooth muscle and promote the disease and its complications. Myeloid cells participate critically in all phases of atherosclerosis from initiation through progression, and ultimately the thrombotic consequences of this disease. Foam cells, lipid-laden macrophages, constitute the hallmark of atheromata. Much of the recent expansion in knowledge of the roles of myeloid cells in atherosclerosis revolves around the functional contributions of subsets of monocytes, precursors of macrophages, the most abundant myeloid cells in the atheroma...
August 2016: Microbiology Spectrum
Tian-Hui An, Quan-Wei He, Yuan-Peng Xia, Sheng-Cai Chen, Suraj Baral, Ling Mao, Hui-Juan Jin, Ya-Nan Li, Meng-Die Wang, Jian-Guo Chen, Ling-Qiang Zhu, Bo Hu
Atherosclerotic plaque vulnerability is the major cause for acute stroke and could be regulated by macrophage polarization. MicroRNA-181b (miR-181b) was involved in macrophage differential. Here, we explore whether miR-181b could regulate atherosclerotic plaque vulnerability by modulating macrophage polarization and the underline mechanisms. In acute stroke patients with atherosclerotic plaque, we found that the serum level of miR-181b was decreased. Eight-week apolipoprotein E knockout (ApoE(-/-)) mice were randomly divided into three groups (N = 10): mice fed with normal saline (Ctrl), mice fed with high-fat diet, and tail vein injection with miRNA agomir negative control (AG-NC)/miR-181b agomir (181b-AG, a synthetic miR-181b agonist)...
October 8, 2016: Molecular Neurobiology
Li-Xue Zhao, Jun-Rong Du, Hong-Jing Zhou, Dong-Ling Liu, Man-Xia Gu, Fang-Yi Long
BACKGROUND: Peroxiredoxins (Prxs) are proposed to function as damage-associated molecular patterns (DAMPs) and contribute to post-ischemic neuroinflammation and brain injury by activating Toll-like receptor (TLR) 4 at the acute and subacute phases after ischemic stroke. However, there are few studies concerning the inflammatory profiles of six distinct subtypes of Prxs (Prx1-Prx6). Our previous study demonstrated that the protective effect of ligustilide (LIG) against cerebral ischemia was associated with inhibition of neuroinflammatory response and Prx/TLR4 signaling in rats...
2016: PloS One
Chin-Yi Cheng, Yu-Chen Lee
Inflammation plays a crucial role in the pathophysiology of acute ischemic stroke. In the ischemic cascade, resident microglia are rapidly activated in the brain parenchyma and subsequently trigger inflammatory mediator release, which facilitates leukocyte-endothelial cell interactions in inflammation. Activated leukocytes invade the endothelial cell junctions and destroy the blood-brain barrier integrity, leading to brain edema. Toll-like receptors (TLRs) stimulation in microglia/macrophages through the activation of intercellular signaling pathways secretes various proinflammatory cytokines and enzymes and then aggravates cerebral ischemic injury...
2016: Evidence-based Complementary and Alternative Medicine: ECAM
Whitney S Gibbs, Rachel A Weber, Rick G Schnellmann, DeAnna L Adkins
AIMS: Determine the subacute time course of mitochondria disruption, cell death, and inflammation in a rat model of unilateral motor cortical ischemic stroke. MAIN METHODS: Rats received unilateral ischemia of the motor cortex and were tested on behavioral tasks to determine impairments. Animals were euthanized at 24h, 72h and 144h and mRNA expression of key mitochondria proteins and indicators of inflammation, apoptosis and potential regenerative processes in ipsilesion cortex and striatum, using RT-qPCR...
September 27, 2016: Life Sciences
Xuyan Jin, Yoo-Jin Shin, Tae-Ryong Riew, Jeong-Heon Choi, Mun-Yong Lee
Slit2, a secreted glycoprotein, has recently been implicated in the post-ischemic astroglial reaction. The objective of this study was to investigate the temporal changes and cellular localization of Slit2 and its receptors, Robo1, Robo2, and Robo4, in a rat transient focal ischemia model induced by middle cerebral artery occlusion. We used double- and triple-immunolabeling to determine the cell-specific changes in Slit2 and its receptors during a 10-week post-ischemia period. The expression profiles of Slit2 and the Robo receptors shared overlapping expression patterns in sham-operated and ischemic striatum...
September 29, 2016: Neurochemical Research
Hendrik H G Hansen, Gert Jan de Borst, Michiel L Bots, Frans L Moll, Gerard Pasterkamp, Chris L de Korte
BACKGROUND AND PURPOSE: Carotid plaque rupture is a major cause of stroke. Key issue for risk stratification is early identification of rupture-prone plaques. A noninvasive technique, compound ultrasound strain imaging, was developed providing high-resolution radial deformation/strain images of atherosclerotic plaques. This study aims at in vivo validation of compound ultrasound strain imaging in patients by relating the measured strains to typical features of vulnerable plaques derived from histology after carotid endarterectomy...
September 29, 2016: Stroke; a Journal of Cerebral Circulation
Priya Revathikumar, Filip Bergqvist, Srividya Gopalakrishnan, Marina Korotkova, Per-Johan Jakobsson, Jon Lampa, Erwan Le Maître
BACKGROUND: The cholinergic anti-inflammatory pathway (CAP) primarily functions through acetylcholine (ACh)-alpha7 nicotinic acetylcholine receptor (α7nAChR) interaction on macrophages to control peripheral inflammation. Interestingly, ACh can also bind α7nAChRs on microglia resulting in neuroprotective effects. However, ACh effects on astrocytes remain elusive. Here, we investigated the effects of nicotine, an ACh receptor agonist, on the cytokine and cholinesterase production of immunocompetent human astrocytes stimulated with interleukin 1β (IL-1β) in vitro...
September 29, 2016: Journal of Neuroinflammation
Steven T W van Haelst, Saskia Haitjema, Jean-Paul P M de Vries, Frans L Moll, Gerard Pasterkamp, Hester M den Ruijter, Gert J de Borst
OBJECTIVE: Diabetes mellitus (DM) is associated with peripheral arterial disease (PAD) and leads to worse clinical outcome compared with patients without DM. The objective of this study was to determine the impact of DM on iliofemoral artery plaque characteristics and to examine secondary clinical outcomes in patients with DM and PAD undergoing surgical revascularization. METHODS: We analyzed 198 patients with and 453 patients without DM from the Athero-Express biobank, a prospective ongoing biobank study, who underwent endarterectomy of the femoral or iliac artery between 2002 and 2013...
September 22, 2016: Journal of Vascular Surgery
Evelyn M R Lake, Paolo Bazzigaluppi, James Mester, Lynsie A M Thomason, Rafal Janik, Mary Brown, JoAnne McLaurin, Peter L Carlen, Dale Corbett, Greg J Stanisz, Bojana Stefanovic
Brain plasticity following focal cerebral ischemia has been observed in both stroke survivors and in preclinical models of stroke. Endogenous neurovascular adaptation is at present incompletely understood yet its potentiation may improve long-term functional outcome. We employed longitudinal MRI, intracranial array electrophysiology, Montoya Staircase testing, and immunofluorescence to examine function of brain vessels, neurons, and glia in addition to forelimb skilled reaching during the subacute stage of ischemic injury progression...
September 21, 2016: NeuroImage
Francesco Petrelli, Mirko Muzzi, Alberto Chiarugi, Giacinto Bagetta, Diana Amantea
Repurposing azithromycin has recently emerged as a promising strategy for the acute treatment of ischemic stroke. The mechanism of neuroprotection depends on the ability of this macrolide to promote polarization of microglia/macrophages towards beneficial M2 phenotypes. The immunomodulatory and anti-inflammatory effects of azithromycin, well documented in chronic inflammatory airway diseases, have been ascribed to the inhibition of the transcription factors nuclear factor (NF)-κB and activator protein (AP)-1...
September 20, 2016: European Journal of Pharmacology
Jin Hwan Lee, Zheng Z Wei, Wenyuan Cao, Soonmi Won, Xiaohuan Gu, Megan Winter, Thomas A Dix, Ling Wei, Shan Ping Yu
Stroke is a leading threat to human life and health in the US and around the globe, while very few effective treatments are available for stroke patients. Preclinical and clinical studies have shown that therapeutic hypothermia (TH) is a potential treatment for stroke. Using novel neurotensin receptor 1 (NTR1) agonists, we have demonstrated pharmacologically induced hypothermia and protective effects against brain damages after ischemic stroke, hemorrhage stroke, and traumatic brain injury (TBI) in rodent models...
September 19, 2016: Neurobiology of Disease
Moon-Sook Woo, Jiwon Yang, Cesar Beltran, Sunghee Cho
Infiltrating monocyte-derived macrophages (M-Mφ) influence stroke-induced brain injury. While the inflammatory nature of M-Mφ in acute stroke has been well documented, their role during the resolution phase of stroke is less clear. With emerging evidence for the involvement of scavenger receptors in innate immunity, this current study addresses a M-Mφ CD36 role in mediating phagocytosis during the recovery phase of stroke. Stroke increases CD36 and TSP-1/2 mRNA levels in ipsilateral hemisphere at acute (3d) and recovery (7d) periods...
September 19, 2016: Journal of Biological Chemistry
Starlee Lively, Sarah Hutchings, Lyanne C Schlichter
Within hours after stroke, potentially cytotoxic pro-inflammatory mediators are elevated within the brain; thus, one potential therapeutic strategy is to reduce them and skew the brain toward an anti-inflammatory state. Because interleukin-4 (IL-4) treatment induces an anti-inflammatory, "alternative-activation" state in microglia and macrophages in vitro, we tested the hypothesis that early supplementation of the brain with IL-4 can shift it toward an anti-inflammatory state and reduce damage after transient focal ischemia...
September 15, 2016: Journal of Neuropathology and Experimental Neurology
Hong-Yan Li, Yan-Yan Su, Yun-Fang Zhang, Zhi-Qiang Liu, Bao-Jun Hua
Ischemia‑reperfusion (I/R) injury is important in the pathogenesis and/or progression of various diseases, including stroke, cardiovascular disease and acute renal injury. Increasing evidence indicates that atorvastatin exerts protective effects in I/R injury‑associated diseases; however, the underlying mechanisms remain to be fully elucidated. In the present study, oxygen‑glucose deprivation (OGD)/reperfusion‑stimulated. RAW264.7 murine macrophages served as a model of I/R injury. The knockdown of peroxisome proliferator activated receptor‑γ (PPARγ) expression in these cells increased OGD/reperfusion‑induced expression of inducible nitric oxide synthase (iNOS), tumor necrosis factor‑α (TNF‑α) and interferon‑γ (IFN‑γ), and enhanced OGD/reperfusion‑induced downregulation of the expression of cluster of differentiation (CD) 206, at the mRNA and protein levels...
September 15, 2016: Molecular Medicine Reports
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 2016: Journal of the American Heart Association
Wen-Jing Xie, Hong-Quan Yu, Yu Zhang, Qun Liu, Hong-Mei Meng
Clinical outcomes are positively associated with hematoma absorption. The monocyte-macrophage scavenger receptor, CD163, plays an important role in the metabolism of hemoglobin, and a soluble form of CD163 is present in plasma and other tissue fluids; therefore, we speculated that serum CD163 affects hematoma absorption after intracerebral hemorrhage. Patients with intracerebral hemorrhage were divided into high- and low-level groups according to the average CD163 level (1,977.79 ± 832.91 ng/mL). Compared with the high-level group, the low-level group had a significantly slower hematoma absorption rate, and significantly increased National Institutes of Health Stroke Scale scores and modified Rankin Scale scores...
July 2016: Neural Regeneration Research
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