Intercellular adhesion molecule‐1‐deficient mice are less susceptible to cerebral ischemia‐reperfusion lnjury

Sg, Soriano; Lipton, Stuart A.; Wang, Yufeng; Xiao, Min; Springer, T.A.; Jc, Gutierrez-Ramos; Pr, Hickey

doi:10.1002/ana.410390511

Cited by 172 publications

(68 citation statements)

References 28 publications

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“…Similar results were obtained in wild-type animals immunodepleted of neutrophils. After (3 hours) MCAO in ICAM-1−/− mice followed by either 21 or 45 hours reperfusion, the ICAM-1−/− mice had a 5.6-fold (at 21 hours) or 7.8-fold (at 45 hours) reduction in cerebral infarct size compared with the wild-type mice (Soriano et al, 1996).…”

Section: Leukocytes and Reperfusionmentioning

confidence: 89%

Cerebral Ischemia and Reperfusion: The Pathophysiologic Concept as a Basis for Clinical Therapy

Schaller

Graf

2004

J Cereb Blood Flow Metab

301

208

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The ischemic penumbra has been documented in the laboratory animal as severely hypoperfused, nonfunctional, but still viable brain tissue surrounding the irreversibly damaged ischemic core. Saving the penumbra is the main target of acute stroke therapy, and is the theoretical basis behind the reperfusion concept. In experimental focal ischemia, early reperfusion has been reported to both prevent infarct growth and aggravate edema formation and hemorrhage, depending on the severity and duration of prior ischemia and the efficiency of reperfusion, whereas neuronal damage with or without enlarged infarction also may result from reperfusion (so-called reperfusion injury). Activated neutrophils contribute to vascular reperfusion damage, yet posthypoxic cellular injury occurs in the absence of inflammatory species. Protein synthesis inhibition occurs in neurons during reperfusion after ischemia, underlying the role that these pathways play in prosurvival and proapoptotic processes that may be differentially expressed in vulnerable and resistant regions of the reperfused brain tissue. Ischemia-induced decreases in the mitochondrial capacity for respiratory activity probably contribute to the ongoing impairment of energy metabolism during reperfusion and possibly also the magnitude of changes seen during ischemia. From these experimental data, the concept of single-drug intervention cannot be effective. Further experimental research is needed, especially of the study of biochemical markers of the injury process to establish the role of several drugs.

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Section: Leukocytes and Reperfusionmentioning

confidence: 89%

Cerebral Ischemia and Reperfusion: The Pathophysiologic Concept as a Basis for Clinical Therapy

Schaller

Graf

2004

J Cereb Blood Flow Metab

301

208

View full text Add to dashboard Cite

show abstract

“…Moreover, in focal ischemia models, anti-leukocyte interventions decrease cerebral edema (Strachan et al, 1992), improve cerebral blood flow (Grogaard et al, 1989;Connolly et al, 1996;Ishikawa et al, 2004), and reduce infarct size (Connolly et al, 1996;Chopp et al, 1994;Beech et al, 2001;Xu et al, 2004;Zheng et al, 2004). Finally, adhesion molecule knockout mice consistently exhibit smaller lesion volumes following focal stroke than their wild-type counterparts (Prestigiacomo et al, 1999;Soriano et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Slit modulates cerebrovascular inflammation and mediates neuroprotection against global cerebral ischemia

Altay

McLaughlin

et al. 2007

Experimental Neurology

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Cerebrovascular inflammation contributes to secondary brain injury following ischemia. Recent in vitro studies of cell migration and molecular guidance mechanisms have indicated that the Slit family of secreted proteins can exert repellant effects on leukocyte recruitment in response to chemoattractants. Utilizing intravital microscopy, we addressed the role of Slit in modulating leukocyte dynamics in the mouse cortical venular microcirculation in vivo following TNFα application or global cerebral ischemia. We also studied whether Slit affected neuronal survival in the mouse global ischemia model as well as in mixed neuronal-glial cultures subjected to oxygenglucose deprivation. We found that systemically administered Slit significantly attenuated cerebral microvessel leukocyte-endothelial adherence occurring 4 h after TNFα and 24 h after global cerebral ischemia. Administration of RoboN, the soluble receptor for Slit, exacerbated the acute chemotactic response to TNFα. These findings are indicative of a tonic repellant effect of endogenous Slit in brain under acute proinflammatory conditions. Three days of continuous systemic administration of Slit following global ischemia significantly attenuated the delayed neuronal death of hippocampal CA1 pyramidal cells. Moreover, Slit abrogated neuronal death in mixed neuronal-glial cultures exposed to oxygen-glucose deprivation. The ability of Slit to reduce the recruitment of immune cells to ischemic brain and to provide cytoprotective effects suggests that this protein may serve as a novel anti-inflammatory and neuroprotective target for stroke therapy.

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“…All animal procedures were approved by the Burnham Administrative Panel on Laboratory Animal Care. Transient middle cerebral artery occlusion (tM-CAO) (Longa et al, 1989;Soriano et al, 1996;Wang et al, 1998) was induced in adult male C57BL/6 mice (25-35 g) under isoflurane anesthesia in a mixture of oxygen and nitrous oxide (30:70). A small incision was made in the neck of an anesthetized mouse and a 6.0 silicone-coated monofilament (Johnson & Johnson) was inserted into the common carotid artery up to the circle of Willis to occlude the ostium of the middle cerebral artery for 60 min.…”

Section: Methodsmentioning

confidence: 99%

Myocyte Enhancer Factor 2C as a Neurogenic and Antiapoptotic Transcription Factor in Murine Embryonic Stem Cells

McKercher²,

Cui³

et al. 2008

Journal of Neuroscience

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Cell-based therapies require a reliable source of cells that can be easily grown, undergo directed differentiation, and remain viable after transplantation. Here, we generated stably transformed murine ES (embryonic stem) cells that express a constitutively active form of myocyte enhancer factor 2C (MEF2CA). MEF2C has been implicated as a calcium-dependent transcription factor that enhances survival and affects synapse formation of neurons as well as differentiation of cardiomyocytes. We now report that expression of MEF2CA, both in vitro and in vivo, under regulation of the nestin enhancer effectively produces "neuronal" progenitor cells that differentiate into a virtually pure population of neurons. Histological, electrophysiological, and behavioral analyses demonstrate that MEF2C-directed neuronal progenitor cells transplanted into a mouse model of cerebral ischemia can successfully differentiate into functioning neurons and ameliorate stroke-induced behavioral deficits.

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Intercellular adhesion molecule‐1‐deficient mice are less susceptible to cerebral ischemia‐reperfusion lnjury

Cited by 172 publications

References 28 publications

Cerebral Ischemia and Reperfusion: The Pathophysiologic Concept as a Basis for Clinical Therapy

Cerebral Ischemia and Reperfusion: The Pathophysiologic Concept as a Basis for Clinical Therapy

Slit modulates cerebrovascular inflammation and mediates neuroprotection against global cerebral ischemia

Myocyte Enhancer Factor 2C as a Neurogenic and Antiapoptotic Transcription Factor in Murine Embryonic Stem Cells

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