A5114374703- Atherosclerosis and Cardiovascular Diseases
- Chemokine receptors and signaling
- Cell Adhesion Molecules Research
- Asthma and respiratory diseases
- Natural product bioactivities and synthesis
- Renin-Angiotensin System Studies
- Adipokines, Inflammation, and Metabolic Diseases
- Receptor Mechanisms and Signaling
- Phytochemistry and Biological Activities
- Inflammatory mediators and NSAID effects
- Nitric Oxide and Endothelin Effects
- Traditional and Medicinal Uses of Annonaceae
- Neuropeptides and Animal Physiology
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Angiogenesis and VEGF in Cancer
- Immune Response and Inflammation
- Lipoproteins and Cardiovascular Health
- Bioactive natural compounds
- Peroxisome Proliferator-Activated Receptors
- Liver Disease Diagnosis and Treatment
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Acute Myocardial Infarction Research
- Plant Physiology and Cultivation Studies
- Hormonal Regulation and Hypertension
- Eicosanoids and Hypertension Pharmacology
Universitat de València
2015-2024
INCLIVA Health Research Institute
2015-2024
Spanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition
2019-2024
Instituto de Salud Carlos III
2009-2024
Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas
2016-2024
Hospital Clínico Universitario de Valencia
2012-2022
Laboratorios Farmaceúticos Rovi (Spain)
2022
Ministry of Health
2007-2021
Menéndez Pelayo International University
2019-2021
Sistemas Genómicos
2016-2018
Neutrophil extracellular traps (NETs) composed of DNA decorated with histones and proteases trap kill bacteria but also injure host tissue. Here we show that during a bloodstream infection methicillin-resistant Staphylococcus aureus, the majority are sequestered immediately by hepatic Kupffer cells, resulting in transient increases liver enzymes, focal ischaemic areas robust neutrophil infiltration into liver. The neutrophils release NETs vasculature, which remain anchored to vascular wall...
Platelet-endothelial cell adhesion molecule-1 (PECAM-1, CD31) plays an active role in the process of leukocyte migration through cultured endothelial cells vitro and anti-PECAM-1 antibodies (Abs) inhibit accumulation leukocytes into sites inflammation vivo. Despite latter, it is still not clear at which stage emigration vivo PECAM-1 involved. To address this point directly, we studied effect Ab, recognizing rat PECAM-1, on responses within mesenteric microvessels using intravital microscopy....
1. A series of flavonoids isolated from Indian medicinal plants: kaempferol-3-O-galactoside, hispidulin, nepetin, scutellarein, scutellarein-7-O-glucuronide, hibifolin and morelloflavone were studied for their activity as inhibitors microsomal lipid peroxidation scavengers oxygen free radicals in vitro well a model xenobiotic toxicity mouse.2. All compounds inhibited vitro. The most potent nepetin (non-enzymic peroxidation) (enzymic with IC50's the micromolar range. Some behaved hydroxyl...
The incidence of cardiovascular diseases in premenopausal women is lower than men or postmenopausal women. This study reports the discovery a low grade systemic inflammation, including monocyte adhesion to arterial endothelium, elicited by menopause estrogen depletion. Chronic treatment with dose 17-beta-estradiol inhibition renin-angiotensin system reduced this inflammation. Using an vitro flow chamber human and venous endothelial cells, we found that leukocytes from healthy were more...
Abstract Endothelial cell senescence is a hallmark of vascular aging that predisposes to disease. We aimed explore the capacity renin–angiotensin system (RAS) heptapeptide angiotensin (Ang)‐(1‐7) counteract human endothelial and identify intracellular pathways mediating its potential protective action. In umbilical vein (HUVEC) cultures, Ang II promoted senescence, as revealed by enhancement in senescence‐associated galactosidase (SA‐β‐gal+) positive staining, total telomeric DNA damage,...
Cardiovascular disease (CVD) remains the leading cause of death and disability worldwide. While many factors can contribute to CVD, atherosclerosis is cardinal underlying pathology, its development associated with several metabolic risk including dyslipidemia obesity. Recent studies have definitively demonstrated a link between low-grade systemic inflammation two relevant abnormalities: hypercholesterolemia Interestingly, both disorders are also endothelial dysfunction/activation,...
Background —Angiotensin II (Ang II) plays a critical role in the development of vascular lesions hypertension, atherosclerosis, and several renal diseases. Because Ang may contribute to leukocyte recruitment associated with these pathological states, aim present study was assess leukocyte–endothelial cell interactions vivo. Methods Results —Intravital microscopy rat mesenteric postcapillary venules used. Sixty minutes superfusion 1 nmol/L induced significant increase rolling flux (83.8±20.7...
ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSynthesis and Pharmacological Evaluation of 2'-Hydroxychalcones Flavones as Inhibitors Inflammatory Mediators GenerationJ. F. Ballesteros, M. J. Sanz, A. Ubeda, Miranda, S. Iborra, Paya, AlcarazCite this: Med. Chem. 1995, 38, 14, 2794–2797Publication Date (Print):July 1, 1995Publication History Published online1 May 2002Published inissue 1 July 1995https://pubs.acs.org/doi/10.1021/jm00014a032https://doi.org/10.1021/jm00014a032research-articleACS...
Angiotensin II (Ang II) is implicated in the development of cardiac ischemic disorders which prominent neutrophil accumulation occurs. Ang can be generated intravascularly by renin-angiotensin system or extravascularly mast cell chymase. In this study, we characterized ability to induce accumulation.Intraperitoneal administration (1 nmol/L) induced significant recruitment within 4 hours (13.3+/-2.3x10(6) neutrophils per rat versus 0.7+/-0.5x10(6) control animals), disappeared 24 hours....
Abstract Angiotensin II (Ang-II) displays inflammatory activity and is implicated in several cardiovascular disorders. This study evaluates the effect of cis- trans (t)-resveratrol (RESV) two vivo models vascular inflammation identifies cardioprotective mechanisms that underlie them. In vivo, Ang-II–induced arteriolar leukocyte adhesion was inhibited by 71% t-RESV (2.1 mg/kg, i.v.), but not affected cis-RESV. Because estrogens influence rennin-angiotensin system, chronic treatment with (15...
Abdominal aortic aneurysm (AAA) is a pathological condition of permanent vessel dilatation that predisposes to the potentially fatal consequence rupture. SGLT-2 (sodium-glucose cotransporter 2) inhibitors have emerged as powerful pharmacological tools for type 2 diabetes mellitus treatment. Beyond their glucose-lowering effects, recent studies shown reduce cardiovascular events and beneficial effects on several vascular diseases such atherosclerosis; however, potential inhibition AAA remain...
Objective— Abdominal aortic aneurysm (AAA) is a vascular disorder characterized by chronic inflammation of the wall. Low concentrations vitamin D 3 are associated with AAA development; however, potential direct effect on remains unknown. This study evaluates oral treatment receptor (VDR) ligand, calcitriol, dissecting induced angiotensin-II (Ang-II) infusion in apoE −/− mice. Approach and Results— Oral calcitriol reduced Ang-II–induced formation mice, which was unrelated to systolic blood...
Abstract Angiotensin II (Ang-II) is associated with atherogenesis and arterial subendothelial mononuclear leukocyte infiltration. We have demonstrated that Ang-II causes the initial attachment of cells to arteriolar endothelium. now report on contribution CC chemokines this response. Intraperitoneal administration 1 nM induced MCP-1, RANTES, MIP-1α generation, maximal at 4 h, followed by recruitment 8 24 h. Using intravital microscopy within rat mesenteric microcirculation h after exposure...
Significance Invariant natural killer T cells (iNKT) have been found primarily patrolling inside blood vessels in the liver, where they respond to bacterial glycolipids presented by CD1d on liver macrophages. We show joint iNKT are localized outside of and directly joint-homing pathogen, Borrelia burgdorferi , which causes Lyme borreliosis using multichannel spinning-disk intravital microscopy. These interacted with B. at vessel wall disrupted its dissemination attempts into joints....
AimsInsulin resistance (IR) is a major risk factor for cardiovascular disease and atherosclerosis. Life-threatening acute events are mainly due to rupture of unstable plaques, the role vascular smooth muscle cells (VSMCs) in this process IR, Type 2 diabetes mellitus, metabolic syndrome (T2DM/MetS) has not been fully addressed. Therefore, VSMC survival generation plaques T2DM/MetS involvement inflammatory mediators was investigated.