Nathalie Burg

ORCID: 0000-0003-1944-8086
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About
Contact & Profiles
Research Areas
  • Sphingolipid Metabolism and Signaling
  • Platelet Disorders and Treatments
  • Cell Adhesion Molecules Research
  • Systemic Lupus Erythematosus Research
  • Cardiac Valve Diseases and Treatments
  • TGF-β signaling in diseases
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Pulmonary Hypertension Research and Treatments
  • Inflammasome and immune disorders
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Eicosanoids and Hypertension Pharmacology
  • Cholesterol and Lipid Metabolism
  • Caveolin-1 and cellular processes
  • Blood disorders and treatments
  • S100 Proteins and Annexins
  • Antiplatelet Therapy and Cardiovascular Diseases
  • Endoplasmic Reticulum Stress and Disease
  • Barrier Structure and Function Studies
  • Renal Diseases and Glomerulopathies
  • Medical Imaging and Pathology Studies
  • Immune Response and Inflammation
  • Periodontal Regeneration and Treatments

Hospital for Special Surgery
2017-2024

Cornell University
2017-2022

Weill Cornell Medicine
2017

Rockefeller University
2004-2016

New York University
2001

New York University Langone Orthopedic Hospital
2001

The vasculature of the central nervous system (CNS) forms a selective barrier termed blood-brain (BBB). Disruption BBB may contribute to various CNS diseases. Conversely, intact restricts efficient penetration CNS-targeted drugs. Here, we report BBB-regulatory role endothelial sphingosine 1-phosphate (S1P) receptor-1, G protein-coupled receptor known promote function in peripheral vessels. Endothelial-specific S1pr1 knockout mice (S1pr1iECKO ) showed breach for small-molecular-mass...

10.1073/pnas.1618659114 article EN Proceedings of the National Academy of Sciences 2017-04-10

Objective Immune complex ( IC ) deposition activates polymorphonuclear neutrophils PMN s), increases vascular permeability, and leads to organ damage in systemic lupus erythematosus rheumatoid arthritis. The bioactive lipid sphingosine 1‐phosphate (S1P), acting via S1P receptor 1 (S1P ), is a key regulator of endothelial cell EC barrier function. This study was undertaken investigate whether augmenting integrity signaling attenuates inflammatory injury mediated by s. Methods In vitro...

10.1002/art.40558 article EN Arthritis & Rheumatology 2018-05-21

In rheumatoid arthritis, inflammatory mediators extravasate from blood into joints via gaps between endothelial cells (ECs), but the contribution of ECs is not known. Sphingosine 1-phosphate receptor 1 (S1PR1), widely expressed on ECs, maintains vascular barrier. Here, we assessed integrity and EC S1PR1 signaling to joint damage in mice exposed serum-induced arthritis (SIA). EC-specific deletion or pharmacological blockade promoted leak amplified SIA, whereas overexpression treatment with an...

10.1172/jci.insight.171467 article EN cc-by JCI Insight 2024-06-09

<h3>Background</h3> Proliferative lupus nephritis (LN) is characterized by robust glomerular and tubulo- interstitial inflammation, sub-endothelial deposits of immunoglobulin, increased endothelial cell permeability. Sphingosine 1- Phosphate Receptor 1 (S1PR1) has multiple protective effects on cells (ECs): it maintains barrier function thereby protecting against vascular leakage, limits the number leukocytes adhering to transmigrating across ECs, protects ECs apoptosis in response...

10.1136/lupus-2022-lupus21century.81 article EN cc-by-nc 2022-12-01
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