A5036275865- Connexins and lens biology
- Nitric Oxide and Endothelin Effects
- Blood Coagulation and Thrombosis Mechanisms
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- X-ray Diffraction in Crystallography
- Heme Oxygenase-1 and Carbon Monoxide
- Thermoregulation and physiological responses
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Cell Adhesion Molecules Research
- Adenosine and Purinergic Signaling
- Neuroscience and Neural Engineering
- Bioactive Compounds and Antitumor Agents
- Nanoparticle-Based Drug Delivery
- Muscle Physiology and Disorders
- Thermal and Kinetic Analysis
- Angiogenesis and VEGF in Cancer
- Cardiomyopathy and Myosin Studies
- Ion Channels and Receptors
- Neuroscience of respiration and sleep
- Computational Drug Discovery Methods
- Crystallization and Solubility Studies
- Receptor Mechanisms and Signaling
- Eicosanoids and Hypertension Pharmacology
- Biochemical effects in animals
- Synthesis and biological activity
Rutgers, The State University of New Jersey
2022-2025
Rutgers New Jersey Medical School
2022-2025
Rutgers Sexual and Reproductive Health and Rights
2024
University of the Americas
2020-2022
Pontificia Universidad Católica de Chile
2016-2021
Austral University of Chile
2016
Abstract S ‐nitrosylation of Cx43 gap junction channels critically regulates communication between smooth muscle cells and endothelial cells. This post‐translational modification also induces the opening undocked hemichannels. However, its specific impact on vasomotor regulation remains unclear. Considering role TRPV4 channel activation in promoting vasodilatation through nitric oxide (NO) production, we investigated direct modulation hemichannels by activation. Using proximity ligation...
The adherens junction complex, composed mainly of vascular endothelial (VE)-cadherin, β-catenin, p120, and γ-catenin, is the main element barrier in postcapillary venules. S-nitrosylation β-catenin p120 an important step proinflammatory agents-induced hyperpermeability. We investigated vitro vivo whether or not VE-cadherin S-nitrosylated using platelet-activating factor (PAF) as agonist. report that PAF-stimulates VE-cadherin, which disrupts its association with β-catenin. In addition, based...
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.
Abstract Objective The endothelium regulates crucial aspects of vascular function, including hemostasis, vasomotor tone, proliferation, immune cell adhesion, and microvascular permeability. Endothelial cells (ECs), especially in arterioles, are pivotal for flow distribution peripheral resistance regulation. Investigating physiology, particularly ECs, demands precise isolation culturing techniques. Methods Freshly isolated ECs vital examining protein expression, ion channel behavior, calcium...
Deletion of pannexin‐1 (Panx‐1) leads not only to a reduction in endothelium‐derived hyperpolarization but also an increase NO‐mediated vasodilation. Therefore, we evaluated the participation Panx‐1‐formed channels control membrane potential and [Ca 2+ ] i endothelial cells. Changes vasodilation, potential, superoxide anion (O 2 ⋅– ) formation, cell were analyzed rat isolated mesenteric arterial beds primary cultures Inhibition Panx‐1 with probenecid (1 mM) or blocking peptide 10 Panx (60 μ...
The synthesis and characterization of the full family 11 pyrazoles were performed by means UV–Vis, FTIR, 1H NMR, 13C two-dimensional NMR experiments DFT simulations. As are known for showing diverse biological actions, they also tested in NCI-60 cancer cell line panel, moderate to good activity against different lines. Furthermore, anti-proinflammatory test a set form (E)-4-((4-bromophenyl)diazenyl)-3,5-dimethyl-1-R-phenyl-1H-pyrazole was performed, this is based on study blockage increase...
ABSTRACT S-nitrosylation of Cx43 gap junction channels critically regulates communication between smooth muscle cells and endothelial cells. This posttranslational modification also induces the opening undocked hemichannels. However, its specific impact on vasomotor regulation remains unclear. Considering role TRPV4 channel activation in promoting vasodilation through nitric oxide (NO) production, we investigated direct modulation hemichannels by activation. Using proximity ligation assay,...
ABSTRACT Connexin-43 (Cx43) plays a critical role in the propagation of action potentials and cardiac contractility. In healthy cardiomyocytes, Cx43 is mainly located at intercalated disk; however, remodeling observed pathologies linked with arrhythmogenesis sudden death. Using mouse model Duchenne muscular dystrophy (DMD), we previously demonstrated that localizes to lateral side dystrophic forming undocked hemichannels. β-adrenergic signaling-induced stress promotes S-nitrosylation opening...
We previously demonstrated that the NO-receptor soluble guanylyl cyclase (GC1) has ability to transnitrosate other proteins in a reaction involves, some cases, oxidized Thioredoxin 1 (oTrx1). This transnitrosation cascade was established
Inflammation disrupts the endothelial barrier and increases microvascular permeability (hyperpermeability), leading to tissue edema. Mechanisms for onset of hyperpermeability have been focus many studies. However, major pathological consequences are related impairment in terminating hyperpermeability, rather than its onset, sustained inflammation. Therefore, we innovatively studying mechanisms involved inactivation restoration normal permeability. We demonstrated that agonist-induced...
Endothelial cells form a permeability barrier to macromolecules that can be modulated in post‐capillary venules through the activation of Ca 2+ ‐dependent signaling pathways by pro‐inflammatory agents, such as platelet‐activating factor (PAF). This depends on release from endoplasmic reticulum and influx extracellular space, which may involved membrane channels formed connexins (i.e. hemichannels) or pannexins. We analyzed participation these PAF‐elicited intracellular concentration ([Ca ] i...
Introduction: Ischemia-reperfusion (I-R) injury is a significant complication in vascular surgery or organ transplantation. I-R involves intracellular Ca2+ overload, nitric oxide (NO), oxidative stress. increases endothelial hyperpermeability leading to tissue edema and damage mediated by increase. The role of permeable channels not defined. Connexin (Cx) proteins form hemichannels, allowing the exchange molecules between extracellular spaces. Cx43 isoform highly expressed cells (EC)....
In resistance arteries, smooth muscle cells (SMCs) and endothelial (ECs) are communicated through gap junctions (i.e. myoendothelial junctions), which provide a signaling pathway for control of vasomotor tone. this context, the Ca 2+ associated to contraction might also be transmitted via activate regulatory feedback mechanism (myoendothelial feedback) by production endothelium‐dependent vasodilators. It is thought that IP 3 main ‐related from cells, but direct contribution not clear. We...
The vascular endothelium regulates vasomotor tone in arterioles through intercellular conduction of electrical signals by gap junctions. Endothelial vasodilation is mediated nitric oxide (NO) and a hyperpolarizing current initiated the endothelium. Both are transmitted to smooth muscle cells evoking relaxation. express connexin (Cx) 37,40,43. Cx hemichannels allow exchange ions molecules between intracellular extracellular compartments that may be associated with endothelial activity....