Proximity of brain infarcts to regions of endogenous neurogenesis and involvement of striatum in ischaemic stroke

Delavaran, Hossein; Sjunnesson, Håkan; Arvidsson, Åke; Lindvall, Olle; Norrving, Bo; Westen, Danielle van; Kokaia, Zaal; Lindgren, Arne

doi:10.1111/j.1468-1331.2012.03877.x

Cited by 33 publications

(27 citation statements)

References 23 publications

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“…The ET-1 model of focal ischemia uses the vasoconstrictor actions of the peptide ET-1 [52, 53]. This peptide causes focal ischemic damage after microinjections into the CNS [54], which is suitable for reproducing the focal strokes frequently occurring in the human brain [55]. In addition, the ET-1 model is easily performed without the complicated surgical procedures of other stroke models like the MCAO intraluminal filament technique, which may induce hyperthermia and other surgical complications [56].…”

Section: Discussionmentioning

confidence: 99%

Neurodegeneration and Glial Response after Acute Striatal Stroke: Histological Basis for Neuroprotective Studies

Lima

Santana

Fernandes

et al. 2016

Oxidative Medicine and Cellular Longevity

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Stroke is a leading cause of death and neurological disability worldwide and striatal ischemic stroke is frequent in humans due to obstruction of middle cerebral artery. Several pathological events underlie damage progression and a comprehensive description of the pathological features following experimental stroke in both acute and chronic survival times is a necessary step for further functional studies. Here, we explored the patterns of microglial activation, astrocytosis, oligodendrocyte damage, myelin impairment, and Nogo-A immunoreactivity between 3 and 30 postlesion days (PLDs) after experimental striatal stroke in adult rats induced by microinjections of endothelin-1 (ET-1). The focal ischemia induced tissue loss concomitant with intense microglia activation between 3 and 14 PLDs (maximum at 7 PLDs), decreasing afterward. Astrocytosis was maximum around 7 PLDs. Oligodendrocyte damage and Nogo-A upregulation were higher at 3 PLDs. Myelin impairment was maximum between 7 and 14 PLDs. Nogo-A expression was higher in the first week in comparison to control. The results add important histopathological features of ET-1 induced stroke in subacute and chronic survival times. In addition, the establishment of the temporal evolution of these neuropathological events is an important step for future studies seeking suitable neuroprotective drugs targeting neuroinflammation and white matter damage.

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Section: Discussionmentioning

confidence: 99%

Neurodegeneration and Glial Response after Acute Striatal Stroke: Histological Basis for Neuroprotective Studies

Lima

Santana

Fernandes

et al. 2016

Oxidative Medicine and Cellular Longevity

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“…It is still not clear whether the neurons in the previous ischemic zone are preexistent cells that can be reactivated by an adequate blood supply or if they are neurons of new origin. Nevertheless, cerebral microvessel remodeling is accompanied by improved neurological behavior [89,90]. …”

Section: Discussionmentioning

confidence: 99%

Remodeling of Cerebral Microcirculation after Ischemia-Reperfusion

Lapi

Colantuoni²

2015

J Vasc Res

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Clinical and experimental studies have been focused on the pathophysiological mechanisms induced by brain ischemia-reperfusion injury. Recovery events, such as neurogenesis, angiogenesis and the growth of new blood vessels from the preexisting vascular tree, have been intensively studied in the last decades to clarify the vascular remodeling crucial for stroke outcome. This review aims to discuss the cerebral microcirculation remodeling induced by ischemia-reperfusion and the mechanisms involved in angiogenesis and vasculogenesis. The first in vivo observations were focused on anastomotic shunting of cerebral blood flow (CBF) in experimental and clinical models. Thereafter, vascular remodeling induced by cerebral ischemia-reperfusion was reported in mice and rats. Successively, other studies have assessed that within 30 days of middle cerebral artery (MCA) occlusion in rats, there is an increase in CBF and recovery from stroke. Recently, rats submitted to transient MCA occlusion showed pial microcirculation remodeling with the formation of new arterioles sprouting from penumbra vessels and overlapping the ischemic core. This review focuses on the production and/or activation of vasculotrophic factors able to trigger and facilitate microvascular remodeling. Vascular endothelial growth factor and endothelium-released nitric oxide appear to be the main factors involved in the formation of new vessels during microvascular remodeling. These studies are fundamental for consequent interventions on molecular targets, useful for fostering vascular remodeling and the recovery of functions.

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“…Cerebral ischemia is known to stimulate neurogenesis [17,18]. Since NSC or progenitor cells are dormant in the adult brain and can be activated by injury.…”

Section: Discussionmentioning

confidence: 99%

Effect of Ilexonin A on the Notch signaling pathway following cerebral ischemia-reperfusion in rats

Han¹,

Zheng²,

Zhang³

et al. 2018

biomedicalresearch

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Proximity of brain infarcts to regions of endogenous neurogenesis and involvement of striatum in ischaemic stroke

Cited by 33 publications

References 23 publications

Neurodegeneration and Glial Response after Acute Striatal Stroke: Histological Basis for Neuroprotective Studies

Neurodegeneration and Glial Response after Acute Striatal Stroke: Histological Basis for Neuroprotective Studies

Remodeling of Cerebral Microcirculation after Ischemia-Reperfusion

Effect of Ilexonin A on the Notch signaling pathway following cerebral ischemia-reperfusion in rats

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