Differences between arterial occlusive and cortical photothrombosis stroke models with magnetic resonance imaging and microtubule-associated protein-2 immunoreactivity

Yushmanov, Victor E.; Kharlamov, Alexander; Simplaceanu, Elena; Williams, Donald S.; Jones, Stephen C.

doi:10.1016/j.mri.2006.04.007

Cited by 7 publications

(7 citation statements)

References 41 publications

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“…Moreover, the variations in ADC i /ADC c within the ischemic area of the brain, although present, were not statistically significant. Several previous reports on the fall in ADC correlated with severity of brain perfusion deficit (8,10,34) owed, probably, to a better MR sensitivity: 1) at 4.7 T compared to 3 T in the present study (8,10), or 2) in a human brain vs. small rat brain (34). Thus, 23 Na slope mapping in the ischemic brain provided better description of the heterogeneity in the ischemic core compared to the ADC mapping in particular experimental setting of our study.…”

Section: Discussionsupporting

confidence: 43%

“…Additional complications include potential permanent or transient (‘pseudonormalization’) ADC reversibility, which may be accompanied by selective neuronal loss in the lesion core after early reperfusion (1,3,7). To better characterize the threshold phenomena resulting in the ADC/CBF mismatch in stroke, the region-specific ADC responses to cerebral perfusion deficit have been described previously in different models of focal ischemia in rats (8–10). Novel MRI approaches to monitor the progression of ischemic damage and refine the detection of the ischemic penumbra include mapping of cerebral metabolic rate of oxygen utilization (11), blood-oxygen-level-dependent MRI (12) and pH-weighted MRI (13).…”

Section: Introductionmentioning

confidence: 99%

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Inhomogeneous sodium accumulation in the ischemic core in rat focal cerebral ischemia by ²³Na MRI

Yushmanov

Kharlamov

Yanovski

et al. 2009

Magnetic Resonance Imaging

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Purpose: To test the hypotheses that (i) the regional heterogeneity of brain sodium concentration ([Na ϩ ] br ) provides a parameter for ischemic progression not available from apparent diffusion coefficient (ADC) data, and (ii) [Na ϩ ] br increases more in ischemic cortex than in the caudate putamen (CP) with its lesser collateral circulation after middle cerebral artery occlusion in the rat. Materials and Methods:23 Na twisted projection MRI was performed at 3 Tesla. [Na ϩ ] br was independently determined by flame photometry. The ischemic core was localized by ADC, by microtubule-associated protein-2 immunohistochemistry, and by changes in surface reflectivity. Results:Within the ischemic core, the ADC ratio relative to the contralateral tissue was homogeneous (0.63 Ϯ 0.07), whereas the rate of [Na ϩ ] br increase (slope) was heterogeneous (P Ͻ 0.005): 22 Ϯ 4%/h in the sites of maximum slope versus 14 Ϯ 1%/h elsewhere (here 100% is [Na ϩ ] br in the contralateral brain). Maximum slopes in the cortex were higher than in CP (P Ͻ 0.05). In the ischemic regions, there was no slope/ADC correlation between animals and within the same brain (P Ͼ 0.1). Maximum slope was located at the periphery of ischemic core in 8/10 animals. Unlike ADC,23 Na MRI detected within-core ischemic lesion heterogeneity. Conclusion:

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Section: Discussionsupporting

confidence: 43%

Section: Introductionmentioning

confidence: 99%

Inhomogeneous sodium accumulation in the ischemic core in rat focal cerebral ischemia by ²³Na MRI

Yushmanov

Kharlamov

Yanovski

et al. 2009

Magnetic Resonance Imaging

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“…These properties make the arterial occlusion model more comparable in size and location to the photothrombotic stroke. Another advantage of comparing this ligation MCAO model to the photothrombotic model is that vascular occlusion is permanent in both (Gonzalez and Kolb, 2003; Yushmanov et al 2006). At low magnification, both types of stroke exhibited a distinct ischemic core area sharply separated from the surrounding non-ischemic tissue restricted to the somatosensory cortex, and not including the striatum (Figure 1).…”

Section: Resultsmentioning

confidence: 99%

“…Whereas in the artery occlusion model the microcirculation is left intact, the photochemical reaction used in the photothrombotic stroke results in broader microvascular injury and loss of capillary flow (Traystman et al, 2003; Yushmanov et al, 2006). This critical difference between the two types of brain damage has implication for stroke outcome and prompted us to investigate the impact of the two types of injury on cell survival and evolution of the infarct.…”

Section: Introductionmentioning

confidence: 99%

Direct comparison of microglial dynamics and inflammatory profile in photothrombotic and arterial occlusion evoked stroke

et al. 2017

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Many focal cerebral ischemia models utilize the middle cerebral artery occlusion (MCAO) evoked by coagulation to induce ischemic damage in the cortex and mimic the pathology observed in human patients. A second, increasingly popular model, the photothrombotic stroke, uses a laser beam to irradiate the MCA after administration of a photosensitizing dye. This widely used procedure is slowly replacing the MCAO model because of the easiness of the surgical protocol and the reproducibility of the damage. However, the photochemical reaction also results in wider microvascular injury. In this study, we have evaluated the impact of these two types of stroke in the cell survival and evolution of stroke, focusing on microglial cells, the first responders to cell injury. Two groups of heterozygote Cx3CR1-GFP reporter mice (to follow microglia) were subject to stroke injury either with coagulator-mediated occlusion or photothrombotic MCA damage. Microglial cells dynamics of activation and phagocytosis together with astrocytic response and leukocyte infiltration were characterized at 1, 3 and 7 days after damage. Photothrombotic stroke delayed microglial and astrocytic invasion of the ischemic core and accumulation of phagocytic microglia. It also elicited higher levels of inflammatory cytokines/chemokines and increased infiltration from the periphery. In addition, only the neurons in the MCAO stroke showed phenotype plasticity by downregulating the transcription factor NeuN. These data provide a better understanding of the exact temporal and spatial dynamics of the inflammatory response in these two animal models of stroke and identify more relevant targets for human therapy.

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“…MAPs make up a class of cytoskeletal proteins essential for the functions of microtubules and are generally believed to serve as microtubule‐connecting links to organelles, vesicles, and other cytoskeletal elements (Shepherd, 1994). MAP2 has also been used as a sensitive marker for brain damage in diverse disease models, including seizures (Ballough et al, 1995), ischemia and hypoxia (Kitagawa et al, 1989; Zhang et al, 1999; Kitano et al, 2004; Yushmanov et al, 2006; Pastori et al, 2007), and contusive brain injuries (Saatman et al, 2006). However, MAP2 was initially established as a marker that disappeared from the damaged neurons, which was detected immunohistochemically and was believed to have very limited use as a clinical diagnostic marker.…”

Section: Discussionmentioning

confidence: 99%

Microtubule‐associated protein 2, an early blood marker of ischemic brain injury

Park

Joo

Lee

et al. 2011

J of Neuroscience Research

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The aim of this study was to develop a sensitive and rapid blood marker to detect ischemic brain injury, because imaging techniques have a limited capacity to identify lesions during the first crucial hours without massive tissue destruction. Rats were subjected to middle cerebral artery occlusion for various durations (0.5-3 hr), followed by reperfusion. At different time points after ischemia and/or ischemia-reperfusion, the amounts of glial fibrillary acidic protein (GFAP) and microtubule-associated protein 2 (MAP2) in the cerebrospinal fluid (CSF) and serum were analyzed by Western blotting. Brain infarction was observed in an ischemia-duration-dependent manner. GFAP was drastically increased in the CSF 24 and 48 hr after reperfusion, without change in the serum level. Serum levels of MAP2 remarkably increased as early as 0.5 hr of ischemia, much earlier than the observation of minimal tissue injury 3 hr following occlusion. The serum MAP2 level was further increased by a short period (2 hr) of reperfusion, even in 0.5- and 1-hr ischemic rats, despite not observing any typical tissue injuries 24 hr after reperfusion. These results indicate that the MAP2 protein may be able to detect early neuronal injuries, because the level of this protein in the blood spikes before the appearance of visible macrolesions. Therefore, MAP2 could potentially be used as a novel early marker for the detection of a neurotoxic insult.

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Differences between arterial occlusive and cortical photothrombosis stroke models with magnetic resonance imaging and microtubule-associated protein-2 immunoreactivity

Cited by 7 publications

References 41 publications

Inhomogeneous sodium accumulation in the ischemic core in rat focal cerebral ischemia by ²³Na MRI

Inhomogeneous sodium accumulation in the ischemic core in rat focal cerebral ischemia by ²³Na MRI

Direct comparison of microglial dynamics and inflammatory profile in photothrombotic and arterial occlusion evoked stroke

Microtubule‐associated protein 2, an early blood marker of ischemic brain injury

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Differences between arterial occlusive and cortical photothrombosis stroke models with magnetic resonance imaging and microtubule-associated protein-2 immunoreactivity

Cited by 7 publications

References 41 publications

Inhomogeneous sodium accumulation in the ischemic core in rat focal cerebral ischemia by 23Na MRI

Inhomogeneous sodium accumulation in the ischemic core in rat focal cerebral ischemia by 23Na MRI

Direct comparison of microglial dynamics and inflammatory profile in photothrombotic and arterial occlusion evoked stroke

Microtubule‐associated protein 2, an early blood marker of ischemic brain injury

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Inhomogeneous sodium accumulation in the ischemic core in rat focal cerebral ischemia by ²³Na MRI

Inhomogeneous sodium accumulation in the ischemic core in rat focal cerebral ischemia by ²³Na MRI