A5075747606- French Urban and Social Studies
- Traumatic Brain Injury and Neurovascular Disturbances
- Neonatal and fetal brain pathology
- Venous Thromboembolism Diagnosis and Management
- Cancer, Hypoxia, and Metabolism
- Retinal and Optic Conditions
- Aging, Elder Care, and Social Issues
- Agriculture and Rural Development Research
- Cardiovascular Health and Disease Prevention
- Angiogenesis and VEGF in Cancer
- Cerebrovascular and Carotid Artery Diseases
- COVID-19 Clinical Research Studies
- Acute Ischemic Stroke Management
- Hemoglobinopathies and Related Disorders
- Neurological Disease Mechanisms and Treatments
- Pregnancy and preeclampsia studies
- Retinal Imaging and Analysis
- Cultural Identity and Heritage
- Neuroinflammation and Neurodegeneration Mechanisms
- Cancer Research and Treatments
- Medieval Architecture and Archaeology
- Archaeological and Historical Studies
- Medieval European Literature and History
- Retinal Diseases and Treatments
- Neonatal Respiratory Health Research
Inserm
2016-2025
Université Paris Cité
2016-2025
Assistance Publique – Hôpitaux de Paris
2016-2025
Hôpital Lariboisière
2016-2025
Sorbonne Paris Cité
2013-2024
Laboratoire de Recherche Vasculaire Translationnelle
2019-2023
Hôpital Bichat-Claude-Bernard
2014-2023
Centre National de la Recherche Scientifique
2003-2023
Laboratoire Architecture Ville Urbanisme Environnement
2011-2023
Université Paris Nanterre
2023
Complicated abdominal aortic aneurysm (AAA) is a major cause of mortality in elderly men. Ang II–dependent TGF-β activity promotes progression experimental Marfan syndrome. However, the role models AAA has not been comprehensively assessed. Here, we show that systemic neutralization breaks resistance normocholesterolemic C57BL/6 mice to II–induced formation and markedly increases their susceptibility disease. These aneurysms displayed large spectrum complications on echography, including...
Perinatal inflammation is a major risk factor for neurological deficits in preterm infants. Several experimental studies have shown that systemic can alter the programming of developing brain. However, these do not offer detailed pathophysiological mechanisms, and they rely on relatively severe infectious or inflammatory stimuli most likely reflect levels observed many human The goal present study was to test hypothesis moderate sufficient white matter development.Newborn mice received...
Abstract Acute myocardial infarction is a common condition responsible for heart failure and sudden death. Here, we show that following acute in mice, CD8 + T lymphocytes are recruited activated the ischemic tissue release Granzyme B, leading to cardiomyocyte apoptosis, adverse ventricular remodeling deterioration of function. Depletion decreases apoptosis within myocardium, hampers inflammatory response, limits injury improves These effects recapitulated mice with B -deficient cells. The...
Increased permeability, predominantly controlled by endothelial junction stability, is an early event in the deterioration of vascular integrity ischemic disorders. Hemorrhage, edema, and inflammation are main features reperfusion injuries, as observed acute myocardial infarction (AMI). Thus, preservation fundamental heart disease. Angiopoietins pivotal modulators cell-cell junctions integrity. We hypothesized that hypoxic induction angiopoietin-like protein 4 (ANGPTL4) might modulate...
Rationale: Optimal outcome after myocardial infarction (MI) depends on a coordinated healing response in which both debris removal and repair of the extracellular matrix play major role. However, adverse remodeling excessive inflammation can promote heart failure, positioning leucocytes as central protagonists potential therapeutic targets tissue wound MI. Objective: In this study, we examined role triggering receptor expressed myeloid cells-1(TREM-1) orchestrating inflammatory that follows...
Acute myocardial infarction (MI) is a severe ischemic disease responsible for heart failure and sudden death. Inflammatory cells orchestrate postischemic cardiac remodeling after MI. Studies using mice with defective mast/stem cell growth factor receptor c-Kit have suggested key roles mast (MCs) in remodeling. Because mutations affect multiple types of both immune nonimmune origin, we addressed the impact MCs on function MI, c-Kit-independent MC-deficient (Cpa3(Cre/+)) mice. In response to...
Cerebrovascular impairment is frequent in patients with Alzheimer disease and believed to influence clinical manifestation severity of the disease. Cardiovascular risk factors, especially hypertension, have been associated higher developing To investigate mechanisms underlying cross talk, we established a mouse model dual pathology by infusing hypertensive doses angiotensin II into transgenic APPPS1 mice overexpressing mutated human amyloid precursor presenilin 1 proteins. At 4.5 months, at...
Rationale: Cerebrovascular function is critical for brain health, and endogenous vascular protective pathways may provide therapeutic targets neurological disorders. S1P (Sphingosine 1-phosphate) signaling coordinates functions in other organs, 1 (S1P receptor-1) modulators including fingolimod show promise the treatment of ischemic hemorrhagic stroke. However, also lymphocyte trafficking, lymphocytes are currently viewed as principal target modulation Objective: To address roles mechanisms...
Patients with sickle-cell disease (SCD) suffer from tissue damage and life-threatening complications caused by vasoocclusive crisis (VOC). Endothelin receptors (ETRs) are mediators of one the most potent vasoconstrictor pathways in mammals, but relationship between vasoconstriction VOC is not well understood. We report here that pharmacological inhibition ETRs prevented hypoxia-induced acute organ a mouse model SCD. An vivo ultrasonographic study renal hemodynamics showed substantial...
By mimicking sympathetic stimulation in vivo, we previously reported that mice globally lacking serotonin 5-HT 2B receptors did not develop isoproterenol-induced left ventricular hypertrophy. However, the exact cardiac cell type(s) expressing (cardiomyocytes versus noncardiomyocytes) involved pathological heart hypertrophy was never addressed vivo. We report here receptor solely cardiomyocytes, like global receptor–null mice, are resistant to and dysfunction, as well increases cytokine...
The structure and function of blood vessels varies along the vascular tree. Endothelial dysfunction is a hallmark increased cardiovascular (CV) risk that can be assessed by several methods, some which are invasive restricted application. aim this study was to determine whether laser Doppler response skin microcirculation acetylcholine, reflects conduit artery brachial flow-mediated dilation (FMD).Noninvasive measurement endothelium-dependent vasodilation in flowmetry (LDF) local transdermal...
Objective— Leukocyte infiltration in ischemic areas is a hallmark of myocardial infarction, and overwhelming innate immune cells has been shown to promote adverse remodeling cardiac rupture. Recruitment inflammatory the heart depends highly on family CC-chemokines their receptors. Here, we hypothesized that chemokine decoy receptor D6, which specifically binds scavenges CC-chemokines, might limit inflammation after infarction. Methods Results— D6 was expressed human murine infarcted...
Sphingosine-1-phosphate (S1P) signaling is essential for vascular development and postnatal homeostasis. The relative importance of S1P sources sustaining these processes remains unclear.To address the level redundancy in bioactive provision to developing mature vasculature.S1P production was selectively impaired mouse platelets, erythrocytes, endothelium, or smooth muscle cells by targeted deletion genes encoding sphingosine kinases -1 -2. deficiency aggregation spreading washed platelets...
Defective systemic and local iron metabolism correlates with cardiac disorders. Hepcidin, a master sensor, actively tunes trafficking. We hypothesized that hepcidin could play key role to locally regulate homeostasis after acute myocardial infarction.Cardiac repair was analyzed in mice harboring specific cardiomyocyte or myeloid cell deficiency of challenged infarction.We found the expression elevated infarction deletion cardiomyocytes failed improve function. However, transplantation bone...
BACKGROUND This study investigated the effects of impairment to placental flow on patterns through aortic isthmus because in fetus, this vascular segment is link between parallel systems perfused by left and right ventricles. METHODS AND RESULTS A progressive increase resistance blood placenta was created seven exteriorized fetal lambs mechanical umbilical vein compression. Blood flows were measured ascending aorta, pulmonary artery, isthmus, artery at baseline each compression level. The...
We recently demonstrated that endogenous nitric oxide (NO) modulates collateral blood flow in a neonatal stroke model rats. The inhalation of NO (iNO) has been found to be neuroprotective after ischemic brain damage adults. Our objective was examine whether iNO could modify cerebral during ischemia-reperfusion and reduce lesions the developing brain.In vivo variations cortical concentrations occurring 20-ppm exposure were analyzed using voltammetric method P7 rat pups. Inhaled NO-mediated...
Gain-of-function mutations in the human WNK1 (with-no-lysine[K]1) gene are responsible for a monogenic form of arterial hypertension, and polymorphisms have been associated with common essential hypertension. The role renal ionic reabsorption has established, but no investigation its possible influence on vascular tone, an determinant blood pressure, performed until now. complete inactivation mouse is embryonically lethal. We, thus, examined Wnk1(+/-) haploinsufficient adult mice whether...
Diabetes increases the risk of stroke by three, related mortality, and delays recovery. We aimed to characterize functional structural alterations in cerebral microvasculature before after experimental ischemia a mouse model type 1 diabetes. hypothesized that preexisting brain microvascular disease patients with diabetes might partly explain increased severity impact on outcome. was induced 4-week-old C57Bl/6J mice intraperitoneal injections streptozotocin (60 mg/kg). After 8 weeks diabetes,...
Background and Purpose— The best conceivable treatment for hypoxia-ischemia (HI) is the restoration of blood flow to hypoxic-ischemic region(s). Our objective was examine whether boosting NO-cGMP signaling using sildenafil citrate, a phosphodiesterase-type 5 inhibitor, could modify cerebral reduce lesions in developing brain. Methods— HI induced P7 Sprague–Dawley rats by unilateral carotid artery occlusion hypoxia, followed either PBS or sildenafil. Blood-flow velocities were measured...