Biology subjects

Lemasson, B.

Publications and source records attributed to Lemasson, B..

3 recordsLinked to original sources

bioRxiv2026

Intermittent Hypoxia Alters Cerebrovascular Recovery After Stroke

Stroke is a prevalent chronic disease, significantly contributing to mortality and long-term disability. The cerebrovascular recovery process after stroke can be complicated by certain comorbidities, including obstructive sleep apnea syndrome (OSA). However, the mechanisms underlying this deleterious impact of OSA on post-stroke recovery remain elusive. We conducted a preclinical study in rats submitted to stroke and intermittent hypoxia (IH), the main characteristic of OSA, to investigate the effects of IH on stroke lesion and to decipher the pathophysiological mechanisms of this stroke-OSA interaction. Using a malonate model of ischemic stroke on Sprague Dawley rats exposed to either normoxia or intermittent hypoxia for over 56 days, we monitored brain lesion size, microvascular plasticity and blood brain barrier (BBB) permeability using in vivo 4.7T-MRI. Finally, we assessed oxidative stress, inflammation, and angiogenesis-related gene expression by qPCR, and NeuN, GFAP, Collagen IV and ZO-1 expression by immunohistological staining. Our findings indicate that while IH does not significantly affect lesion volume reduction over time, it exacerbates ischemic injury-induced necrosis and neuronal loss. Additionally, IH amplifies post-stroke inflammation, as evidenced by increased IL-6 and TGF-{beta} expression, and induces oxidative stress by increasing DHE staining and decreasing Superoxide Dismutase (SOD1) level. Vascular assessment revealed IH-induced modifications in vessel radius and angiogenic factors expression (VEGF, Ang2), alongside increased BBB permeability and altered expression of aquaporin 1 and claudin 1, particularly in the acute phase post-stroke. These results suggest that IH alters cerebrovascular integrity and exacerbates inflammatory response following ischemic stroke, potentially contributing to poorer long-term functional outcomes. Understanding the mechanisms through which IH exacerbates post-stroke injury may guide the development of targeted neuroprotective strategies to improve stroke recovery in patients with OSA.

pathology↗

bioRxiv2025

Multimodal Characterization and Evolution of Malonate-induced Stroke Model: advanced MRI, Histology-Molecular Profiling

BackgroundIschemic stroke is a leading cause of mortality and disability worldwide, yet therapeutic options remain limited. Preclinical models play a crucial role in understanding stroke pathophysiology and evaluating potential treatments. This study aimed to provide a comprehensive characterization of the temporal evolution of ischemic injury induced by malonate intracerebral injection using multiparametric magnetic resonance imaging (MRI) combined with histological and molecular analysis. MethodsFocal ischemic lesions were induced by malonate injection in the striatum of rats. Lesion volume was monitored using T2-weighted MRI at multiple time points (Day 1, D7, D14, D28, and D56). Water content, reflecting vasogenic edema, was assessed via apparent diffusion coefficient (ADC) measurements, while vascular alterations were evaluated using blood volume fraction (BVF), vessel radius, and oxygen saturation (StO2). Blood-brain barrier (BBB) permeability was quantified through gadolinium-enhanced MRI. Molecular analyses by RT-qPCR were conducted to assess oxidative stress, inflammation, and angiogenesis-related gene expression. Immunohistological staining was performed to investigate neuronal loss, astrocytic activation, and vascular remodeling. ResultsMRI analysis showed a significant and progressive decrease in lesion volume. Water content increased from D4 onward. Ischemic injury significantly altered vascular function, leading to increased vessel radius and BVF while reducing tissue oxygenation. BBB permeability was elevated at D7 and D56, accompanied by increased claudin-1 and aquaporin-1 expression. Molecular analysis revealed an upregulation of inflammatory markers (IL-6, TGF-{beta}, NF-{kappa}B), oxidative stress response genes (SOD1, Nrf1), and impaired angiogenesis with increased Ang1/Ang2 but reduced VEGF/VEGFR1. Immunohistological analysis demonstrated neuronal loss, astrocytic activation, and vascular remodeling, characterized by increased ZO-1 and ColI-IV expression. ConclusionThe observed changes in lesion volume, vascular function, inflammation, oxidative stress, and angiogenesis highlight key mechanisms underlying post-stroke recovery. These findings emphasize the importance of long-term monitoring in preclinical stroke models and may contribute to the development of novel therapeutic strategies.

neuroscience↗

bioRxiv2018

From: Benjamin LemassonParametric response mapping as a new MRI approach for the characterization of posttraumatic cerebral edema

PurposeCerebral edema is usually assessed with mean ADC value obtained with MRI. We aimed to use parametric response mapping (PRM), a voxel-based analysis, in a rat model of traumatic brain injury (TBI) to characterize the cerebral edema and to compare findings to those obtained with the classical global mean ADC analysis. Ultimately we wished to test whether early PRM analysis could identify the vasogenic or cellular edematous pattern two hours after trauma.\n\nMaterials and MethodsExperiments were conducted in a rat model of TBI in accordance with French Government guidelines. Eighteen traumatic brain-injured rats (TBI group) were compared to 7 sham-operated rats (Sham group). Diffusion-weighted images were acquired before and immediately (H0), 60min (H1) and 120min (H2) after the trauma. Two regions of interest (ROI) including cortex (cortical-ROI) and the whole brain (brain-ROI) were manually delineated.\n\nResultsAveraged ADC value in cortical-ROI was significantly reduced at H2 in the TBI group versus Sham group (715{+/-}24 vs 781{+/-}16 m2/sec; p=0.04), not in brain-ROI (748{+/-}27 vs 801{+/-}18 m2/sec; p=0.32). By contrast, PRM values were significantly changed in these two ROIs at as soon as H1 in the TBI group (27.5{+/-}4% of the voxels beyond the PRM threshold in TBI group vs 5.1{+/-}1% in sham group; p<0.01). PRM was able to identify the nature of post traumatic cerebral edema: vasogenic, cellular or mixed pattern. ADC data obtained immediately after TBI and analyzed using PRM correlated with ADC data obtained at H2.\n\nConclusionThe PRM approach is more sensitive than averaged ADC at detecting and identifying post-traumatic brain edema. It is able to PRM might be a promising tool to individualize the management of patients with posttraumatic brain edema.

neuroscience↗