Juan Hidalgo

ORCID: 0000-0003-0921-1122
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About
Contact & Profiles
Research Areas
  • Trace Elements in Health
  • Heavy Metal Exposure and Toxicity
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Adipose Tissue and Metabolism
  • Alzheimer's disease research and treatments
  • Iron Metabolism and Disorders
  • Exercise and Physiological Responses
  • RNA regulation and disease
  • Adipokines, Inflammation, and Metabolic Diseases
  • Cytokine Signaling Pathways and Interactions
  • Immune Response and Inflammation
  • Stress Responses and Cortisol
  • Drug Transport and Resistance Mechanisms
  • S100 Proteins and Annexins
  • Vitamin C and Antioxidants Research
  • Pancreatitis Pathology and Treatment
  • Pharmacological Effects of Medicinal Plants
  • Mitochondrial Function and Pathology
  • T-cell and B-cell Immunology
  • Tryptophan and brain disorders
  • Regulation of Appetite and Obesity
  • Immune Cell Function and Interaction
  • Neuroscience and Neuropharmacology Research
  • Environmental Toxicology and Ecotoxicology
  • Neurogenesis and neuroplasticity mechanisms

Universitat Autònoma de Barcelona
2016-2025

Universidad Nacional de Córdoba
2022

Institute of Animal Physiology of the Slovak Academy of Sciences
2017-2019

Universitat de Barcelona
2005-2019

Neurosciences Institute
2002-2018

Institute of Immunology and Physiology
2015-2018

Salk Institute for Biological Studies
2017

University of South Florida
2017

Scripps Research Institute
1998-2017

University of Kentucky
2017

Whether B cells serve as antigen-presenting (APCs) for activation of pathogenic T in the multiple sclerosis model experimental autoimmune encephalomyelitis (EAE) is unclear. To evaluate their role APCs, we engineered mice selectively deficient MHC II on (B–MHC II−/−), and to distinguish this function from antibody production, created transgenic (Tg) that express myelin oligodendrocyte glycoprotein (MOG)–specific cell receptor (BCR; IgHMOG-mem) but cannot secrete antibodies. B–MHC II−/− were...

10.1084/jem.20130699 article EN cc-by-nc-sa The Journal of Experimental Medicine 2013-12-09

Significance Chronic low-grade inflammation is a key driver of metabolic syndrome. This inflammatory response mediated by immune-cell infiltration and the expression cytokines. IL6 implicated in this response, but physiological role signaling unclear. Here, we demonstrate that source influences nature response. We report secreted myeloid cells inhibits adipose tissue macrophage (ATM) accumulation canonical mechanism, adipocytes or muscle promotes ATM noncanonical mechanism. These...

10.1073/pnas.1920004117 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2020-01-24

IL-6 is implicated in the pathogenesis of various neuroinflammatory and neurodegenerative disorders CNS. signals via binding to either membrane bound IL-6Rα (classic signaling) or soluble (s)IL-6Ra (trans-signaling) that then form a complex with gp130 activate JAK/STAT signaling pathway. The importance classic versus trans-signaling mediating actions living CNS relatively unknown was focus this investigation. Bigenic mice (termed GFAP-IL6/sgp130 mice) were generated CNS-restricted,...

10.1523/jneurosci.2830-13.2014 article EN cc-by-nc-sa Journal of Neuroscience 2014-02-12

Abstract Spatiotemporal regulation of tumor immunity remains largely unexplored. Here we identify a vascular niche that controls alternative macrophage activation in glioblastoma (GBM). We show tumor-promoting macrophages are spatially proximate to GBM-associated endothelial cells (ECs), permissive for angiocrine-induced polarization. ECs as one the major sources interleukin-6 (IL-6) expression GBM microenvironment. Furthermore, reveal colony-stimulating factor-1 and angiocrine IL-6 induce...

10.1038/s41467-018-03050-0 article EN cc-by Nature Communications 2018-02-02

Expression of brown adipose tissue (BAT) associated proteins like uncoupling protein 1 (UCP1) in inguinal WAT (iWAT) has been suggested to alter iWAT metabolism. The aim this study was investigate the role interleukin-6 (IL-6) exercise training and cold exposure-induced UCP1 expression. effect daily intraperitoneal injections IL-6 (3 ng/g) C57BL/6 mice for 7 days on expression examined. In addition, determined response 3 exposure (4°C) 5 weeks wild type (WT) whole body knockout (KO) mice....

10.1371/journal.pone.0084910 article EN cc-by PLoS ONE 2014-01-08

In eukaryotic cells, different organelles interact at membrane contact sites stabilized by tethers. Mitochondrial mitofusin 2 (MFN2) acts as a tether that interacts with an unknown partner on the endoplasmic reticulum (ER). this work, we identified MFN2 splice variant ERMIT2 ER tethering of MFN2. Splicing produced and ERMIN2, two ER-specific variants. ERMIN2 regulated morphology, whereas localized ER-mitochondria interface interacted mitochondrial mitofusins to mitochondria. This allowed...

10.1126/science.adh9351 article EN Science 2023-06-22

Abstract Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by anti-nuclear autoantibodies whose production promoted autoreactive T follicular helper (TFH) cells. During SLE pathogenesis, basophils accumulate in secondary lymphoid organs (SLO), amplify autoantibody and progression through mechanisms that remain to be defined. Here, we provide evidence for a direct functional relationship between TFH cells during both humans mice. PD-L1 upregulation on IL-4 are...

10.1038/s41467-024-47691-w article EN cc-by Nature Communications 2024-04-22

The aim of the present study was to test hypothesis that peroxisome proliferator activated receptor-gamma coactivator (PGC) 1alpha is required for exercise-induced adaptive gene responses in skeletal muscle. Whole body PGC-1alpha knockout (KO) and littermate wild-type (WT) mice performed a single treadmill-running exercise bout. Soleus white gastrocnemius (WG) were obtained immediately, 2 h, or 6 h after exercise. Another group KO WT 5-wk training. Soleus, WG, quadriceps approximately 37...

10.1152/ajpendo.00666.2007 article EN AJP Endocrinology and Metabolism 2007-12-12

Mitochondria are critical for cellular bioenergetics, and they mediate apoptosis within cells. We used whole body peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) knockout (KO) animals to investigate its role on organelle function, apoptotic signaling, cytochrome-c oxidase activity, an indicator of mitochondrial content, in muscle other tissues (brain, liver, pancreas). Lack PGC-1alpha reduced content all muscles (17-44%; P < 0.05) but had no effect brain,...

10.1152/ajpcell.00070.2009 article EN AJP Cell Physiology 2009-05-14

A number of intracellular proteins that are protective after brain injury classically thought to exert their effect within the expressing cell. The astrocytic metallothioneins (MT) one example and act via free radical scavenging heavy metal regulation, in particular zinc. Indeed, we have previously established MTs required for successful healing. Here provide evidence a fundamentally different mode action relying upon intercellular transfer from astrocytes neurons, which turn leads...

10.1074/jbc.m708446200 article EN cc-by Journal of Biological Chemistry 2008-03-12

Given the numerous health benefits of exercise, understanding how exercise capacity is regulated a question paramount importance. Circulating interleukin 6 (IL-6) levels surge during and IL-6 favors capacity. However, neither cellular origin circulating nor means by which this cytokine enhances has been formally established yet. Here we show through genetic that majority detectable originates from muscle to increase capacity, must signal in osteoblasts favor osteoclast differentiation...

10.1172/jci133572 article EN Journal of Clinical Investigation 2020-02-20

Abnormal hematopoiesis advances cardiovascular disease by generating excess inflammatory leukocytes that attack the arteries and heart. The bone marrow niche regulates hematopoietic stem cell proliferation hence systemic leukocyte pool, but whether affects organ's microvasculature is unknown. Here we show hypertension, atherosclerosis myocardial infarction (MI) instigate endothelial dysfunction, leakage, vascular fibrosis angiogenesis in marrow, altogether leading to overproduction of...

10.1038/s44161-021-00002-8 article EN cc-by Nature Cardiovascular Research 2021-12-23

Injury to the central nervous system (CNS) elicits an inflammatory response involving activation of microglia, brain macrophages, and astrocytes, processes likely mediated by release proinflammatory cytokines. In order determine role interleukin-6 (IL-6) during in following disruption blood-brain barrier (BBB), we examined effects a focal cryo injury fronto-parietal cortex interleukin-6-deficient (IL-6-/-) normal (IL-6+/+) mice. IL-6+/+ mice, resulted appearance macrophages reactive...

10.1002/(sici)1098-1136(19990215)25:4<343::aid-glia4>3.0.co;2-v article EN Glia 1999-02-15

In order to determine the role of neuropoietic cytokine interleukin-6 (IL-6) during first 3 weeks after a focal brain injury, we examined inflammatory response, oxidative stress and neuronal survival in normal interleukin-6-deficient (knockout, IL-6KO) mice subjected cortical freeze lesion. mice, injury was followed by reactive astrogliosis recruitment macrophages from 1 day postlesion (dpl), peaking at 3–10 dpl, 20 dpl transient immunoreactions were decreased, glial scar present. IL-6KO...

10.1002/1098-1136(200012)32:3<271::aid-glia70>3.0.co;2-5 article EN Glia 2000-01-01

To characterize the physiological role of metallothioneins I and II (MT-I+II) in brain, we have examined chronological effects a freeze injury to cortex normal MT-I+II null mice. In mice, microglia/macrophage activation astrocytosis were observed areas surrounding lesion site, peaking at approximately 1 3 d postlesion (dpl), respectively. At 20 dpl, parenchyma had regenerated. Both brain macrophages astrocytes increased immunoreactivity, dpl it was similar that unlesioned situ hybridization...

10.1523/jneurosci.19-07-02535.1999 article EN cc-by-nc-sa Journal of Neuroscience 1999-04-01
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