Annabel F. Valledor

ORCID: 0000-0003-4232-2633
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About
Contact & Profiles
Research Areas
  • Cholesterol and Lipid Metabolism
  • Drug Transport and Resistance Mechanisms
  • Immune cells in cancer
  • interferon and immune responses
  • Immune Response and Inflammation
  • NF-κB Signaling Pathways
  • Peroxisome Proliferator-Activated Receptors
  • Cytokine Signaling Pathways and Interactions
  • Inflammasome and immune disorders
  • Estrogen and related hormone effects
  • Cancer, Lipids, and Metabolism
  • Immune Cell Function and Interaction
  • Protein Tyrosine Phosphatases
  • Inflammation biomarkers and pathways
  • Atherosclerosis and Cardiovascular Diseases
  • Protein Kinase Regulation and GTPase Signaling
  • Cell death mechanisms and regulation
  • Immunotherapy and Immune Responses
  • Cancer-related gene regulation
  • Steroid Chemistry and Biochemistry
  • Antibiotic Resistance in Bacteria
  • PI3K/AKT/mTOR signaling in cancer
  • Fibroblast Growth Factor Research
  • Adenosine and Purinergic Signaling
  • Hormonal Regulation and Hypertension

Universitat de Barcelona
2015-2024

Institut de Biomedicina de la Universitat de Barcelona
2018-2023

Centro de Investigación Biomédica en Red
2012

Wihuri Research Institute
2012

Universitat Autònoma de Barcelona
2012

Finnish Institute for Health and Welfare
2012

University of Maryland, College Park
2012

Institute for Research in Biomedicine
2007

University of California, San Diego
2003-2004

Barcelona Biomedical Research Park
2003-2004

PPARα, β/δ, and γ regulate genes involved in the control of lipid metabolism inflammation are expressed all major cell types atherosclerotic lesions. In vitro studies have suggested that PPARs exert antiatherogenic effects by inhibiting expression proinflammatory enhancing cholesterol efflux via activation liver X receptor–ABCA1 (LXR-ABCA1) pathway. To investigate potential importance these activities vivo, we performed a systematic analysis β, agonists on foam-cell formation atherosclerosis...

10.1172/jci18730 article EN Journal of Clinical Investigation 2004-12-01

Liver X receptors (LXRs) regulate the expression of genes involved in cholesterol and fatty acid homeostasis, including for ATP-binding cassette transporter A1 (ABCA1) sterol response element binding protein 1 (SREBP1). Loss LXR leads to derepression ABCA1 gene macrophages intestine, while SREBP1c remains transcriptionally silent. Here we report that high-density-lipoprotein (HDL) levels are increased LXR-deficient mice, suggesting possibly other target selected tissues is sufficient result...

10.1128/mcb.23.16.5780-5789.2003 article EN Molecular and Cellular Biology 2003-07-31

Microbe-macrophage interactions play a central role in the pathogenesis of many infections. The ability some bacterial pathogens to induce macrophage apoptosis has been suggested contribute their elude innate immune responses and successfully colonize host. Here, we provide evidence that activation liver X receptors (LXRs) retinoid (RXRs) inhibits apoptotic macrophages colony-stimulating factor (M-CSF) withdrawal several inducers apoptosis. In addition, combined LXR RXR protected from caused...

10.1073/pnas.0407749101 article EN Proceedings of the National Academy of Sciences 2004-12-15

Macrophages exert potent effector functions against invading microorganisms but constitute, paradoxically, a preferential niche for many bacterial strains to replicate. Using model of infection by Salmonella Typhimurium, we have identified molecular mechanism regulated the nuclear receptor LXR that limits host macrophages through transcriptional activation multifunctional enzyme CD38. agonists reduced intracellular levels NAD+ in CD38-dependent manner, counteracting pathogen-induced changes...

10.1016/j.celrep.2017.01.007 article EN cc-by-nc-nd Cell Reports 2017-01-01

Bone marrow-derived macrophages proliferate in response to specific growth factors, including macrophage colony-stimulating factor (M-CSF). When stimulated with activating such as lipopolysaccharide (LPS), stop proliferating and produce proinflammatory cytokines. Although triggering opposed responses, both M-CSF LPS induce the activation of extracellular-regulated kinases (ERKs) 1 2. However, time-course ERK is different; maximal by occurred after 5 15 min stimulation, respectively....

10.1074/jbc.275.10.7403 article EN cc-by Journal of Biological Chemistry 2000-03-01

Abstract Macrophages perform essential functions in the infection and resolution of inflammation. IFN-γ is main endogenous macrophage Th1 type activator. The classical signaling pathway involves activation Stat-1. However, has also capability to activate members MAPK family. In primary bone marrow-derived macrophages, we have observed strong p38 at early time points stimulation, whereas weak ERK-1/2 JNK-1 was detected a more delayed stage. parallel, exerted repressive effects on expression...

10.4049/jimmunol.180.7.4523 article EN The Journal of Immunology 2008-04-01

Osteoclasts are bone-resorbing cells that important for maintenance of bone remodeling and mineral homeostasis. Regulation osteoclast differentiation activity is the pathogenesis treatment diseases associated with loss. Here, we demonstrate retinoid X receptors (RXRs) key elements transcriptional program differentiating osteoclasts. Loss RXR function in hematopoietic resulted formation giant, nonresorbing osteoclasts increased mass male mice protected female from loss following ovariectomy,...

10.1172/jci77186 article EN Journal of Clinical Investigation 2015-01-08

Lipopolysaccharide (LPS) is a powerful stimulator of macrophages and induces apoptosis in these cells. Using primary cultures bone marrow-derived macrophages, we found that the autocrine production tumor necrosis factor-α (TNF-α) has major function LPS-induced apoptosis. LPS activates PKC regulates different mitogen-activated protein kinases (MAPK). We aimed to determine its involvement either secretion TNF-α or induction specific inhibitors mice with gene for PKCϵ disrupted, TNF-α-dependent...

10.1152/ajpcell.00228.2003 article EN AJP Cell Physiology 2003-11-01

C. Cervera, M. Fernández‐Ruiz, A. Valledor, L. Linares, Antón, Ángeles Marcos, G. Sanclemente, I. Hoyo, F. Cofán, M.J. Ricart, Pérez‐Villa, Navasa, T. Pumarola, Moreno. Epidemiology and risk factors for late infection in solid organ transplant recipients. Transpl Infect Dis 2011: 13: 598–607. All rights reserved Background Information concerning the outcome of (LI) after transplantation (SOT) still remains scarce. Methods We prospectively analyzed all patients undergoing SOT from July 2003...

10.1111/j.1399-3062.2011.00646.x article EN Transplant Infectious Disease 2011-04-27

Reprogramming of immunosuppressive tumor-associated macrophages (TAMs) presents an attractive therapeutic strategy in cancer. The aim this study was to explore the role macrophage CD5L protein TAM activity and assess its potential as a target.Monoclonal antibodies (mAbs) against recombinant were raised by subcutaneous immunization BALB/c mice. Peripheral blood monocytes isolated from healthy donors stimulated with IFN/LPS, IL4, IL10, conditioned medium (CM) different cancer cell lines...

10.1016/j.ebiom.2023.104555 article EN cc-by-nc-nd EBioMedicine 2023-04-11

LPS induces in bone marrow macrophages the transient expression of mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1). Because MKP-1 plays a crucial role attenuation different MAPK cascades, we were interested characterization signaling mechanisms involved control LPS-stimulated macrophages. The induction was blocked by genistein, tyrosine inhibitor, and two C (PKC) inhibitors (GF109203X calphostin C). We had previously shown that express isoforms PKC beta I, epsilon, zeta. Of all...

10.4049/jimmunol.164.1.29 article EN The Journal of Immunology 2000-01-01

Liver X receptors (LXRs) exert key functions in lipid homeostasis and control of inflammation. In this study we have explored the impact LXR activation on macrophage response to endogenous inflammatory cytokine IFN-γ. Transcriptional profiling studies demonstrate that ∼38% IFN-γ-induced transcriptional is repressed by macrophages. LXRs also mediated inhibitory effects selected genes primary microglia a model neuroinflammation vivo. resulted reduced STAT1 recruitment promoters tested without...

10.4049/jimmunol.1201393 article EN The Journal of Immunology 2013-05-18

Abstract IL-18 is a member of the IL-1 family involved in innate immunity and inflammation. Deregulated levels are pathogenesis multiple disorders including inflammatory metabolic diseases, yet relatively little known regarding its regulation. Liver X receptors or LXRs key modulators macrophage cholesterol homeostasis immune responses. Here we show that LXR ligands negatively regulate LPS-induced mRNA protein expression bone marrow-derived macrophages. Consistent with this being an...

10.1038/srep25481 article EN cc-by Scientific Reports 2016-05-06

Metal limitation is a common situation during infection and can have profound effects on the pathogen's success. In this report, we examine role of zinc in expression virulence factor uropathogenic Escherichia coli. The pyelonephritis isolate J96 carries two hlyCABD operons that encode RTX toxin α-hemolysin. While coding regions both are largely conserved, upstream sequences, including promoters, unrelated. We show here differently regulated. hly II operon efficiently silenced presence...

10.1038/s41598-018-24964-1 article EN cc-by Scientific Reports 2018-04-19
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