A5087551058- Nitric Oxide and Endothelin Effects
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Adipose Tissue and Metabolism
- Cardiac Ischemia and Reperfusion
- Neonatal and fetal brain pathology
- Cardiac Fibrosis and Remodeling
- Birth, Development, and Health
- Electron Spin Resonance Studies
- Cardiovascular Health and Risk Factors
- Mitochondrial Function and Pathology
- Cardiovascular Disease and Adiposity
- Eicosanoids and Hypertension Pharmacology
- Cancer, Hypoxia, and Metabolism
- Calcium signaling and nucleotide metabolism
- Autophagy in Disease and Therapy
- Atherosclerosis and Cardiovascular Diseases
Rhode Island Hospital
2013-2023
Brown University
2013-2023
Providence College
2013-2016
University of Chicago
2012
Age-associated decline in cardiovascular function is believed to occur from the deleterious effects of reactive oxygen species (ROS). However, failure recent clinical trials using antioxidants patients with disease, and findings showing paradoxical role for NADPH oxidase-derived ROS endothelial challenge this long-held notion against ROS. Here, we examine endothelium-specific conditional increase on coronary function. We have generated a novel binary (Tet-ON/OFF) transgenic mouse...
There are conflicting reports on the role of reactive oxygen species (ROS) i.e. beneficial vs. harmful, in vascular endothelium. Here, we aim to examine whether duration exposure ROS and/or subcellular levels responsible for apparently paradoxical effects oxidants We have recently generated binary (Tet-ON/OFF) conditional transgenic mice (Tet-Nox2:VE-Cad-tTA) that can induce 1.8 ± 0.42-fold increase NADPH oxidase (NOX)-derived specifically endothelium upon withdrawal tetracycline from...
Introduction Increased ROS is associated with vascular pathology. Recent reports showed that whereas short-term (4 weeks) increase in NADPH oxidase-derived endothelium (EC)-specific improved coronary endothelial function, long-term (16+ had adverse effects. Hypothesis We tested the hypothesis (4-8 induces AMPK-FOXO1-mediated expression of SOD2 and thus exert protective effects on EC mitochondria; contrast, (16-20 results nitrotyration inactivation MnSOD, mitochondrial membrane potential...
Introduction: Increase in reactive oxygen species (ROS) is often associated with vascular pathophysiological conditions. Our recent findings demonstrated that transient increase ROS improved coronary endothelial function. However, long-term effects of endothelium-specific on function are not known. Hypothesis: The short-term (four to eight weeks) versus the (16 20 NADPH oxidase-derived will have differential endothelium. Methods: binary (Tet-ON/OFF) conditional transgenic mouse...
Objective Elevated Reactive Oxygen Species (ROS) in Endothelial Cells (EC's) have been implicated the pathogenesis of cardiovascular diseases, and much research has gone into elucidating mechanisms through which oxidative stress leads to these diseases. Research last decade, however, uncovered central role lower levels ROS play physiological intracellular signaling pathways, such as those stimulated by Vascular Growth Factor (VEGF) Tumour Necrosis Factor‐α (TNF‐α) EC's. Our objective this...
Introduction: Increased ROS is often associated with vascular pathology. Recent findings demonstrated that increases in NADPH oxidase-derived endothelium (EC)-specific improved coronary endothelial function by activating AMPK-eNOS signaling pathway. Here, we examined the effects of EC-ROS on vessel density post-infarct ischemic myocardium. Hypothesis: We tested hypothesis increased induces AMPK-FOXO1-mediated overexpression mitochondrial antioxidant MnSOD, which turn has protective Methods:...
Introduction: Failure of several multi-center clinical trials using antioxidants to improve outcomes in patients with cardiovascular disease, and the recent findings showing paradoxical role for NADPH oxidase-derived reactive oxygen species (ROS) endothelial function challenge a long-held notion that higher ROS levels are harmful vascular function. Hypothesis: We examined hypothesis endothelium-specific conditional increase will induce stress-signal-mediated activation eNOS thus coronary...
Rats with a 90‐min left middle cerebral artery occlusion followed by 24‐hour reperfusion (MCAO), pressor responses during muscle contractions were attenuated, as glutamate in the rostral ventrolateral medulla (RVLM) and caudal VLM (CVLM), but GABA increased RVLM CVLM (Brain Res. 2002: 952). This study determined effects of L‐arginine (L‐Arg), nitric oxide (NO) precursor, within or on cardiovascular activity glutamate/GABA levels static exercise left‐sided MCAO rats. Microdialysis L‐Arg into...