To determine the molecular mechanism of cerebral ischemia/reperfusion injury, we examined the microRNA (miRNA) expression profile in rat cortex after focal cerebral ischemia/reperfusion injury using miRNA microarrays and bioinformatic tools to systematically analyze Gene Ontology (GO) function classifications, as well as the signaling pathways of genes targeted by these differentially expressed miRNAs. Our results show significantly changed miRNA expression profiles in the reperfusion period after focal cerebral ischemia, with a total of 15 miRNAs up-regulated and 44 miRNAs down-regulated. Target genes of these differentially expressed miRNAs were mainly involved in metabolic and cellular processes, which were identified as hub nodes of a miRNA-GO-network. The most correlated pathways included D-glutamine and D-glutamate metabolism, the renin-angiotensin system, peroxisomes, the PPAR signaling pathway, SNARE interactions in vesicular transport, and the calcium signaling pathway. Our study suggests that miRNAs play an important role in the pathological process of cerebral ischemia/reperfusion injury. Understanding miRNA expression and function may shed light on the molecular mechanism of cerebral ischemia/reperfusion injury.
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http://dx.doi.org/10.4103/1673-5374.170302 | DOI Listing |
Gene
January 2025
Shengli Clinical Medical College of Fujian Medical University, Fuzhou, Fujian, China; Department of Neurology, Fujian Provincial Hospital, Fuzhou, Fujian, China; Fujian Key Laboratory of Medical Analysis, Fujian Academy of Medical Sciences, Fuzhou, Fujian, China. Electronic address:
Background: Ischemic stroke (IS) is an important disease causing death and disability worldwide, and further investigation of IS-related genes through genome-wide association study (GWAS) data is valuable.
Methods: The study included GWAS data from 62,100 IS patients of European origin and 1,234,808 controls in a cross-tissue transcriptome association study (TWAS). A joint analysis was first performed by the Unified Test for Molecular Markers (UTMOST) and FUSION methods.
Eur Stroke J
January 2025
Department of Neuroradiology, University Hospital Basel, Basel, Switzerland.
Background: There are limited therapeutic options in cases of failed reperfusion (modified thrombolysis in cerebral infarction [mTICI] score < 2b) after stent-retriever and/or aspiration based endovascular treatment (EVT) for acute ischemic stroke. Despite the absence of data supporting its use, rescue therapy (balloon angioplasty and/or stent implantation) is often utilized in such cases. Studies are limited to large vessel occlusions, while the outcomes and complications after rescue therapy in medium/distal vessel occlusions (MDVOs) have not been reported.
View Article and Find Full Text PDFJ Stroke Cerebrovasc Dis
January 2025
Department of Gerontology, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, 646000, China. Electronic address:
Objective: Hirudin has shown potential in promoting angiogenesis and providing neuroprotection in ischemic stroke; however, its therapeutic role in promoting cerebrovascular angiogenesis remains unclear. In this study, we aimed to investigate whether hirudin exerts neuroprotective effects by promoting angiogenesis through the regulation of the Wnt/β-catenin signaling pathway.
Methods: An in vitro model of glucose and oxygen deprivation/reperfusion (OGD/R) was established using rat brain microvascular endothelial cells (BMECs).
Alzheimers Dement
December 2024
STEM Neurology & Neuropsychological0 Research Group Egypt (SNRGE), Port Said, Port Said, Egypt.
Background: The olfactory mucosa cells are capable of lifelong neurogenesis providing a viable source of progenitor cells. Olfactory mucosa progenitor cells (OMPCs) have alleviated several cerebral ischemia/reperfusion damage markers. OMPCs are safely obtainable from the upper nasal cavity.
View Article and Find Full Text PDFJ Med Chem
January 2025
Department of Neurology, the Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, China.
The death signaling complex comprising extrasynaptic NMDAR and TRPM4 plays a pivotal role in the pathogenesis of ischemic stroke. Targeting the protein-protein interactions between NMDAR and TRPM4 represents a promising therapeutic strategy for ischemic stroke. Herein, we describe the discovery of a novel series of NMDAR/TRPM4 interaction interface inhibitors aimed at enhancing neuroprotective efficacy and optimizing pharmacokinetic profiles.
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