Project description:Genome wide DNA methylation profiling of normal and ischemic stroke patients blood samples. The Illumina Infinium 850k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpGs in liquid. Samples included 3 healthy people blood samples, 3 ischemic stroke patients blood samples.
Project description:We performed a genome-wide methylation study in whole-blood DNA from 404 ischemic stroke patient cohort, distributed across 3 ischemic stroke subtypes: Large-artery atherosclerosis (n=132), Small-artery disease (n=141) and Cardio embolic (n=127) . Illumina HumanMethylation450 BeadChip array was used to measure DNA methylation in CpG sites. We performed a genome-wide methylation study in whole-blood DNA from 185 ischemic stroke patient cohort. Illumina HumanMethylation450 BeadChip array was used to measure DNA methylation in CpG sites.
Project description:The purpose of this project was to elucidate gene expression in the peripheral whole blood of acute ischemic stroke patients to identify a panel of genes for the diagnosis of acute ischemic stroke. Peripheral blood samples were collected in Paxgene Blood RNA tubes from stroke patients who were >18 years of age with MRI diagnosed ischemic stroke and controls who were non-stroke neurologically healthy. The results suggest a panel of genes can be used to diagnose ischemic stroke, and provide information about the biological pathways involved in the response to acute ischemic stroke in humans. Total RNA extracted from whole blood in n=39 ischemic stroke patients compared to n=24 healthy control subjects.
Project description:The purpose of this project was to elucidate gene expression in the peripheral whole blood of acute ischemic stroke patients to identify a panel of genes for the diagnosis of acute ischemic stroke. Peripheral blood samples were collected in Paxgene Blood RNA tubes from stroke patients who were >18 years of age with MRI diagnosed ischemic stroke and controls who were non-stroke neurologically healthy. The results suggest a panel of genes can be used to diagnose ischemic stroke, and provide information about the biological pathways involved in the response to acute ischemic stroke in humans.
Project description:Ischemic stroke can be classified depending on its etiology as cardioembolic (CE), large-vessel atheroesclerotic (LAA), lacunar, other or cryptogenic. Our aim was to identify gene expression changes that could differentiate CE and LAA stroke in order to guide the optimal secondary treatment .
Project description:Analysis of microglial gene expression profiles after ischemic stroke. Stroke is a complicated disease caused by the interaction of multiple celltypes. Results provide new insights into the molecular mechanisms underlying microglial activation after ischemic stroke.
Project description:Analysis of astrocytic gene expression profiles after ischemic stroke. Stroke is a complicated disease caused by the interaction of multiple celltypes. Results provide new insights into the molecular mechanisms underlying astrocytic activation after ischemic stroke.
Project description:Many hospitals lack facilities for accurate diagnosis of acute ischemic stroke (AIS). Circular RNA (circRNA) is highly expressed in the brain and is closely associated with stroke. In this study, we examined whether the blood-borne circRNAs can be promising candidates as adjunctive diagnostic biomarkers and their pathophysiological roles after stroke. We profiled the blood circRNA expression in mice subjected to experimental focal cerebral ischemia, and validated the selected circRNAs in AIS patients. We demonstrated that 128, 198 and 789 circRNAs were significantly altered at 5 min, 3 h and 24 h after ischemic stroke, respectively.
Project description:Neurovascular impairments and neuroimmune deregulation contribute to injury progression after ischemic stroke. Dickkopf-1 (DKK1) elevated levels correlates with poor stroke outcomes. DKK1 antagonizes the canonical Wnt pathway that plays a critical role in regulating neurovascular and neuroimmune functions. Herein, we report that DKK1 expression in the normal adult brain is absent, but is de novo expressed at the lesion site after experimental ischemic stroke. Using genetic tools to conditionally induce DKK1 expression in a tissue-specific manner, we reveal that its early induction aggravates neurological deficits and injury severity after stroke, associated with altered neuronal and vascular functions. DKK1 post-stroke induction hinders lesion containment by disorganizing the astroglial scar, leading to a chronic neuroinflammation and increased anxiety-like behaviors. Using chimeric mice, we unravel that DKK1 is released by bone marrow-derived cells (BMDCs) expressing myeloid markers that infiltrate the lesion site. DKK1 restricted induction in BMDCs is sufficient to mediate astroglial scar disorganization. Notably, neutralization of DKK1 limits injury progression and improves neurological recovery after stroke. Our findings indicate that BMDCs-derived DKK1 promotes injury progression after stroke and suggest that neutralizing its biological activity represent a promising therapeutic avenue for ischemic stroke.