A5045556607- Nitric Oxide and Endothelin Effects
- Redox biology and oxidative stress
- Blood Coagulation and Thrombosis Mechanisms
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cell Adhesion Molecules Research
- Ion channel regulation and function
- Genetics, Aging, and Longevity in Model Organisms
- Circadian rhythm and melatonin
- Invertebrate Immune Response Mechanisms
- Adipokines, Inflammation, and Metabolic Diseases
- Barrier Structure and Function Studies
- Ion Transport and Channel Regulation
- Acute Ischemic Stroke Management
- Economic and Social Development
- Polyamine Metabolism and Applications
- Chemical Synthesis and Analysis
- Signaling Pathways in Disease
- Ion Channels and Receptors
- Cardiac Ischemia and Reperfusion
Rutgers New Jersey Medical School
2011-2023
Rutgers, The State University of New Jersey
2011-2023
Mercy University
2021-2023
Pontificia Universidad Católica de Chile
2009-2012
Austral University of Chile
2012
Texas A&M Health Science Center
2012
The methionine sulfoxide reductase system has been implicated in aging and protection against oxidative stress. This conserved reverses the oxidation of residues within proteins. We analyzed one components this system, A gene, Caenorhabditis elegans. found that msra-1 gene is expressed most tissues, particularly intestine nervous system. Worms carrying a deletion are more sensitive to stress, show chemotaxis locomotory defects, 30% decrease median survival. established expression decreases...
Endothelial adherens junction proteins constitute an important element in the control of microvascular permeability. Platelet-activating factor (PAF) increases permeability to macromolecules via translocation endothelial nitric oxide synthase (eNOS) cytosol and stimulation eNOS-derived signaling cascade. The mechanisms by which regulates at junctions are still incompletely understood.We explored hypothesis that PAF stimulates hyperpermeability S-nitrosation (SNO) proteins.We measured...
Termination of microvascular hyperpermeability has been so far accepted to be a passive result the removal applied proinflammatory agonists. We provide in vivo and vitro evidence that 1) inactivation is an actively regulated process, 2) agonists (PAF VEGF) stimulate initiate endothelial mechanisms terminate hyperpermeability, 3) eNOS location-translocation critical activation-inactivation cascade hyperpermeability.
Approaches to reduce excessive edema due the microvascular hyperpermeability that occurs during ischemia-reperfusion (I/R) are needed prevent muscle compartment syndrome. We tested hypothesis cAMP-activated mechanisms actively restore barrier integrity in postischemic striated muscle. found, using I/R intact muscles and hypoxia-reoxygenation (H/R, an mimic) human endothelial cells (HMVECs), can be deactivated by increasing cAMP levels through application of forskolin. This effect was seen...
Nitric oxide (NO) is a key factor in inflammation. Endothelial nitric synthase (eNOS), whose activity increases after stimulation with proinflammatory cytokines, produces NO endothelium. activates two pathways:
Endothelial hyperpermeability is a hallmark of inflammation. barrier function restored after period hyperpermeability, but the mechanisms that deactivate are largely unknown. Exchange protein activated by cAMP (Epac) emerging as possible deactivating/restorative factor in endothelium. Epac localization, which modulated Ezrin/Radixin/Moesin (ERM) proteins, may determine its due to cellular compartmentalization signaling. We report preliminary results testing hypothesis ERM proteins facilitate...
Venular hyperpermeability to macromolecules is a hallmark of inflammation. Platelet‐activating factor (PAF) pro‐inflammatory agent that increases permeability by stimulating endothelial nitric oxide synthase (eNOS) activity and (NO) production, which can either activate soluble guanylyl cyclase (sGC) and/or induce protein S‐nitrosation. Because the thioredoxin (Trx)/thioredoxin reductase (TrxR) system reverse S‐nitrosation, we studied significance S‐nitrosation Trx/TrxR on in human...
Protein S‐nitrosation has emerged recently as a mechanism to regulate cell function. We tested the hypothesis that cytosolic thioredoxin (Trx1) – reductase (TrxR1) system contributes control of endothelial permeability. In human microvascular cells (HMVEC) dermal origin, we used PAF‐stimulated hyperpermeability and hypoxia‐reoxygenation test models. Inhibition Trx1/TrxR1 elevated baseline permeability, allowed further increase in permeability by PAF. PAF increased global reported anti...
Inflammation is characterized by an increase in endothelial barrier permeability (hyperpermeability) to macromolecules. Major efforts have focused on understanding the mechanisms involved hyperpermeability response of cells; however, less attention has been given restoration vascular integrity following hyperpermeability. Because many negative effects are due its persistence beyond what required for preserving organ function, we investigating that terminate and thereby restore microvascular...