Transcriptomic data from a non-human primate model of stroke reproducing endovascular thrombectomy
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PROVIDER: PRJNA1196436 | ENA |
REPOSITORIES: ENA
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Project description:Background and purpose: Rodent models have demonstrated the key pathogenic role of the lectin pathway (LP) of complement activation in brain ischemic injury. Here we assessed the LP activation and its association with stroke severity and outcome in a well-characterized model of stroke mimicking mechanical thrombectomy in non-human primates. Methods: Transient middle cerebral artery occlusion was performed in Macaca fascicularis randomly allocated in cyclosporine A or placebo group. Neurological status was serially assessed. The occlusion lesion, the ischemic penumbra, the final lesion, the lesion growth between occlusion and day 7 as well as the blood-brain barrier permeability using quantitative transfer constant Ktrans ratio and inflammation by quantitative [11C]PK11195 imaging were assessed using positron emission tomography–magnetic resonance (PET-MRI) imaging. Functional residual LP-specific C3b deposition assay was performed in plasma. C3b/iC3b, mannose binding lectin (MBL), MBL associated serine proteases-2 (MASP-2) and interleukin-6 were measured in plasma, cerebrospinal fluid and brain homogenates. Brain tissue was used to perform immunofluorescence and confocal analyses (C3b/iC3b, MBL and MASP-2 and glycocalyx) as well as transcriptomic analysis. Results: Twenty-three subjects were included with a mean age of 6.7 +/- 0.5 years. LP residual activation in plasma collected late after recanalization was significantly decreased compared to baseline conditions. C3b/iC3b peaked at day 7 and this increase correlated with a more severe neurological deficit at day 1 and day 7, a larger final lesion and lesion growth volumes as well as a greater Ktrans ratio. C3b/iC3b, MBL and MASP-2 were found in microvascular thrombi at day 30. At this time point, 760 genes were differentially expressed within the lesion, including 13 LP-related genes. Conclusions: Our results support that the LP of complement activation is involved in thromboinflammation in a non-human primate model of stroke mimicking mechanical thrombectomy in humans.
2025-07-01 | GSE283970 | GEO
Project description:The proteome of cerebral thrombi from patients recanalized by mechanical thrombectomy in an acute phase of stroke was carried out to determine biomarkers of stroke radio-clinical outcomes for stroke physicians (clinical outcome and mortality at 3 months, intracranial hemorrhagic transformation, etc.). Proteome of cerebral thrombi was also used to elucidate stroke physiopathology (paradoxical effect of glucose in acute phase of stroke) and evaluate recanalization treatments (intravenous thrombolysis by rt-PA and/or thrombectomy efficiency). ThrombiOMIC database was incremented by proteomic analyses of cerebral thrombi successfully retrieved from all consecutive stroke patients (n=59) with large vessel occlusion treated by mechanical thrombectomy in acute phase between October 2018 and August 2019 in the intensive care stroke unit of the University Hospital of Nice (France).
2024-01-28 | PXD048837 | Pride
Project description:The proteome of cerebral thrombi from patients recanalized by mechanical thrombectomy in an acute phase of stroke was carried out to determine biomarkers of stroke radio-clinical outcomes for stroke physicians (clinical outcome and mortality at 3 months, intracranial hemorrhagic transformation, etc.). Proteome of cerebral thrombi was also used to elucidate stroke physiopathology (paradoxical effect of glucose in acute phase of stroke) and evaluate recanalization treatments (intravenous thrombolysis by rt-PA and/or thrombectomy efficiency). Retro-MATISSE (Molecular Analysis of Thrombus in Ischemic Stroke prognosiS and Etiology) database was incremented by proteomic analyses of cerebral thrombi successfully retrieved from all consecutive stroke patients (n=47) with large vessel occlusion treated by mechanical thrombectomy in acute phase between December 2020 and May 2021 in the intensive care stroke unit of the University Hospital of Marseille (France).
2024-01-28 | PXD048933 | Pride
Project description:Stroke is a devastating disease. Endovascular mechanical thrombectomy is dramatically changing the management of acute ischemic stroke, raising new challenges regarding brain outcome and opening up new avenues for brain protection. In this context, relevant experiment models are required for testing new therapies and addressing important questions about infarct progression despite successful recanalization, reversibility of ischemic lesions, blood-brain barrier disruption and reperfusion damage. Here, we developed a minimally invasive non-human primate model of cerebral ischemia (Macaca fascicularis) based on an endovascular transient occlusion and recanalization of the middle cerebral artery (MCA). We evaluated per-occlusion and post-recanalization impairment on PET-MRI, in addition to acute and chronic neuro-functional assessment. Voxel-based analyses between per-occlusion PET-MRI and day-7 MRI showed two different patterns of lesion evolution: "symptomatic salvaged tissue" (SST) and "asymptomatic infarcted tissue" (AIT). Extended SST was present in all cases. AIT, remote from the area at risk, represented 45% of the final lesion. This model also expresses both worsening of fine motor skills and dysexecutive behavior over the chronic post-stroke period, a result in agreement with cortical-subcortical lesions. We thus fully characterized an original translational model of ischemia-reperfusion damage after stroke, with consistent ischemia time, and thrombus retrieval for effective recanalization.
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Project description:In this project, we developed an endovascular medical device. To evaluate its biocompatibility, the device (experimental) or a clinical medical device (control) was co-cultured with human immune cells. We further conducted single-cell RNA sequencing to examine potential immunogenic responses at the cellular level.
2025-12-15 | GSE312793 | GEO
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Project description:In the past decade, noble gases have emerged as highly promising neuroprotective agents. Previous studies have demonstrated the efficacy of argon neuroprotection in rodent models of cerebral ischemia. The objective of the present pre-clinical study was to confirm the neuroprotective effect of argon in a non-human primate model of endovascular ischemic stroke. Thirteen adult Macaca mulatta were subjected to a focal cerebral ischemia induced by a transient (90 min) middle cerebral artery occlusion (tMCAO). The monkeys were randomly allocated to a control group (n = 8) and an argon group (n = 5). Pre-mixed gas (40-60 oxygen-argon) was applied 30 min after the onset of tMCAO to 30 min after reperfusion. Infarct volumes were measured from the MRI scans conducted 1 hour and 1 month after the reperfusion. A clinical neurological assessment was performed 24 hours and 1 month after tMCAO. Our results show that Argon dramatically reduced ischemic core volume after ischemia compared to the control group with a long-lasting improvement of post-stroke infarct volume at 1 month. In addition, the neurological scale suggests a better prognosis in argon-treated animals without reaching the significance threshold. These pre-clinical results in gyrencephalic non-human primates support the potential use of this therapeutic approach for future clinical studies.
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Project description:We have developed an endovascular catheter-based device for sampling of the endothelium, intended for RNA-seq analysis. With an outer diameter of 0.23 mm it is capable of reaching peripheral vessels for endothelial sampling, and favourably compares to other approaches with stent retrievers or similar tools. Here, we have collected samples from liver and kidney vessels from swine and performed RNA-sequencing to validate the sample quality.
2022-08-21 | GSE197756 | GEO