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Molecular Advances in Ischemia-Reperfusion Injury in the Brain

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 2157

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Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy
Interests: biochemistry; molecular mechanism; oxidative stress; endometriosis
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Special Issue Information

Dear Colleagues,

Stroke is an acute onset disturbance of cerebral function due to ischemia or hemorrhage. Ischemic stroke is the 3rd leading cause of mortality globally and the number one cause of disability. Two approaches have been pursued to reduce the disease burden of stroke—neuroprotection and reperfusion. Current research is intensively searching for novel therapeutic strategies and is increasingly focusing on the sub-acute and chronic phases after stroke because more patients might be eligible for therapeutic interventions in a prolonged time window. These delayed mechanisms include important pathophysiological pathways such as post-stroke inflammation, apoptosis, angiogenesis, neuronal plasticity, and regeneration. In order to analyze these mechanisms and subsequently evaluate novel drug targets, experimental stroke models with clinical relevance, low mortality, and high reproducibility are sought after. Among these models, middle cerebral artery occlusion (MCAO) using an intraluminal filament has been the most widely used because it achieves minimally invasive injury, is easy to perform, and results in reproducible infarct lesions. In this Special Issue, we welcome research articles and reviews on the molecular pathways involved in ischemic stroke.

Dr. Roberta Fusco
Guest Editor

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Keywords

  • ischemic stroke
  • middle cerebral artery occlusion
  • in vivo model
  • molecular pathway
  • apoptosis
  • oxidative stress
  • inflammation

Published Papers (1 paper)

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Research

20 pages, 2521 KiB  
Article
The Duration of Oxygen and Glucose Deprivation (OGD) Determines the Effects of Subsequent Reperfusion on Rat Pheochromocytoma (PC12) Cells and Primary Cortical Neurons
by Ayesha Singh and Ruoli Chen
Int. J. Mol. Sci. 2023, 24(8), 7106; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24087106 - 12 Apr 2023
Cited by 1 | Viewed by 1759
Abstract
Reperfusion is the fundamental treatment for ischaemic stroke; however, many ischaemic stroke patients cannot undergo reperfusion treatment. Furthermore, reperfusion can cause ischaemic reperfusion injuries. This study aimed to determine the effects of reperfusion in an in vitro ischaemic stroke model—oxygen and glucose deprivation [...] Read more.
Reperfusion is the fundamental treatment for ischaemic stroke; however, many ischaemic stroke patients cannot undergo reperfusion treatment. Furthermore, reperfusion can cause ischaemic reperfusion injuries. This study aimed to determine the effects of reperfusion in an in vitro ischaemic stroke model—oxygen and glucose deprivation (OGD) (0.3% O2)—with rat pheochromocytoma (PC12) cells and cortical neurons. In PC12 cells, OGD resulted in a time-dependent increase in cytotoxicity and apoptosis, and reduction in MTT activity from 2 h onwards. Reperfusion following shorter periods (4 and 6 h) of OGD recovered apoptotic PC12 cells, whereas after 12 h, OGD increased LDH release. In primary neurons, 6 h OGD led to significant increase in cytotoxicity, reduction in MTT activity and dendritic MAP2 staining. Reperfusion following 6 h OGD increased the cytotoxicity. HIF-1a was stabilised by 4 and 6 h OGD in PC12 cells and 2 h OGD onwards in primary neurons. A panel of hypoxic genes were upregulated by the OGD treatments depending on the duration. In conclusion, the duration of OGD determines the mitochondrial activity, cell viability, HIF-1a stabilization, and hypoxic gene expression in both cell types. Reperfusion following OGD of short duration is neuroprotective, whereas OGD of long duration is cytotoxic. Full article
(This article belongs to the Special Issue Molecular Advances in Ischemia-Reperfusion Injury in the Brain)
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