As oligodendrocyte precursor cells (OPCs) are vulnerable to ischemia, their differentiation to oligodendrocytes (OLG) is impaired in chronic cerebral hypoperfusion. Astrocyte–OLG interaction is important for white matter homeostasis. Recently, reactive astrocytes were separated into two types, A1 (cytotoxic) and A2 (neurotrophic). However, their role in prolonged cerebral hypoperfusion remains unclear. We analyzed the effects of interaction between A1–A2 astrocytes and OPC–OLG under hypoperfusion, focusing on mitochondrial migration. As an in vivo model, chronic hypoperfusion model mice were created by bilateral common carotid artery stenosis (BCAS) using microcoils. As a matching in vitro study, rat primary cells were cocultured with a nonlethal concentration of CoCl2. At 28 days after hypoperfusion, the number of OPC and astrocytes increased, whereas that of OLG decreased. Increased astrocytes were mainly A1‐like astrocytes; however, the number of A2‐like type decreased. In cell culture, OPC differentiation was interrupted under mimic chronic ischemia, but improved after astrocyte‐conditioned medium (ACM) was added. However, injured‐ACM was unable to improve OPC maturation. Incubation with CoCl2 changed astrocytes from A2‐like to A1‐like, and mitochondrial migration was also reduced. A Trkβ agonist was able to maintain astrocytes from A1‐like to A2‐like even under hyperperfused conditions, and aided in OPC maturation and memory impairment via mitochondrial migration and drug effects in cell culture study and BCAS model. The reduction of A1‐like astrocytes protects against white matter injury. Trkβ agonists may play an important role in the impairment under chronic ischemic conditions. Mitochondrial migration may be a broad therapeutic strategy for cerebrovascular diseases.Main pointsProlonged cerebral hypoperfusion leads to impaired oligodendrocyte (OLG) maturation and increased numbers of A1 astrocytes. Mitochondria migration maintained A2 astrocyte morphology, mature OLG, and myelinated white matter in vivo/vitro.
We report two cases of proximal posterior cerebral artery (PCA) aneurysms treated with endovascular parent artery occlusion (PAO) with coils. In both cases, selective injection from the 4 F distal access catheter clearly showed the perforating arteries arising from the PCA. Case No 1, a 49-year-old woman, was successfully treated with preservation of a paramedian artery. Case No 2, a 54-year-old woman, was treated in the same manner. The patient underwent extensive thalamic infarction after the procedure because of paramedian artery occlusion. Endovascular PAO with coils is feasible for proximal PCA aneurysms; however, preservation of perforating arteries arising from the PCA is mandatory.
We herein describe a rare case of intraventricular hemorrhage (IVH) due to a distal anterior choroidal artery (AChA) aneurysm associated with an arteriovenous malformation (AVM) in the trigone of the lateral ventricle during early pregnancy. Case Presentation: At 8 weeks of pregnancy, a 36-year-old woman developed sensory aphasia and mild right hemiparesis due to a left lateral IVH. Digital subtraction angiography showed a peripherally located aneurysm branching from the medial perforating branch (MPB) of the plexal segment in the AChA associated with a micro-AVM in the trigone of the left lateral ventricle. Endovascular embolization was performed. A microcatheter was guided to a feeder branching out from the MPB. The aneurysm and the nidus, including the feeder, were occluded by 20% n-butyl-2cyanoacrylate (NBCA). However, right homonymous hemianopsia was apparent postoperatively, although the blood flow of the cisternal segment was preserved. Head MRI showed an acute infarction in the perfusion area of the AChA, including the internal capsule and optic radiation. Conclusion: We performed endovascular embolization to temporarily treat both the aneurysm and the nidus because the source of bleeding was unclear considering the hematoma position and angiographic features. Ischemic complications of the embolization for the aneurysm and the nidus with the preservation of the cisternal segment of the AChA are unusual. Keywords▶ intraventricular hemorrhage, distal anterior choroidal artery aneurysm, arteriovenous malformation This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives International License.
Introduction: Astrocytes play broad roles in the Central nervous system, and are involved in the regulation of cerebral metabolism and blood flow. Normal astrocytes (A2) protect against oxidative stress and excitotoxicity, but unhealthy astrocytes (A1) may release deleterious factors. Oligodendrocytes (OLGs) differentiate from oligodendrocyte-precursor-cells (OPCs) for myelination in white matter, but OPC were vulnerable for ischemia. Therefore, differentiation is impaired when white matter injury occurs in a chronic cerebral hypoperfusion model. Thus, we examined the effects of the interaction between astrocyte and oligodendrocyte lineage cells on myelination focused on mitochondrial migration. Method: A microcoil was applied to the bilateral common carotid arteries in male C57BL/6 mice as an in vivo cerebral chronic hypoperfusion model (BCAS model). A nonlethal concentration of CoCl 2 was added to the primary cell culture from the postnatal rat cortex and incubated in vitro. Results: White matter injury progressed in the BCAS model as myelin decreased. The numbers of OPCs and astrocytes increased after the operation, whereas that of OLGs decreased at day 28. Increased astrocytes were mainly A1 type, and A2 type were decreased. OPC differentiation was disrupted under the stressed conditions in the cell culture, but improved after administration of astrocyte-conditioned medium (ACM), but injured ACM couldn’t improve maturation. Incubate with CoCl 2 change astrocyte A2 to A1, and mitochondrial migration also reduced. Trkβ agonist could change astrocyte A1 to A2 even in hyperperfused condition, and also help OPC maturation via mitochondrial migration and drug effect in vivo and in vitro. Conclusions: The reduction in incrementing A1 astrocytes protect white matter injury. and Trkβ agonist may play an important role in the impairment under chronic ischemic conditions. Mitochondrial migration could be a broad therapeutic strategy for cerebrovascular disorders.
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