A5054391881- Neurogenesis and neuroplasticity mechanisms
- Neuroinflammation and Neurodegeneration Mechanisms
- Mesenchymal stem cell research
- Multiple Sclerosis Research Studies
- Retinoids in leukemia and cellular processes
- Mitochondrial Function and Pathology
- MicroRNA in disease regulation
- Parkinson's Disease Mechanisms and Treatments
- Stress Responses and Cortisol
- interferon and immune responses
- Spinal Dysraphism and Malformations
- Epigenetics and DNA Methylation
- Neurogenetic and Muscular Disorders Research
- Alzheimer's disease research and treatments
- Vitamin D Research Studies
- Immune Response and Inflammation
- Genetics and Neurodevelopmental Disorders
- Immune cells in cancer
- Reproductive System and Pregnancy
- Cytokine Signaling Pathways and Interactions
- RNA modifications and cancer
- Barrier Structure and Function Studies
Universidad de Navarra
2020
University of Cambridge
2015-2019
Consorci Institut D'Investigacions Biomediques August Pi I Sunyer
2010-2019
Wellcome/MRC Cambridge Stem Cell Institute
2015-2019
Medical Research Council
2015
Stem Cell Institute
2015
Background Demyelination and axonal damage are critical processes in the pathogenesis of multiple sclerosis (MS). Oxidative stress pro-inflammatory cytokines elicited by inflammation mediates tissue damage. Methods/Principal Findings To monitor demyelination injury associated with microglia activation we employed a model using cerebellar organotypic cultures stimulated lipopolysaccharide (LPS). Microglia activated LPS released (IL-1β, IL-6 TNFα), increased expression inducible nitric oxide...
The mechanisms regulating differentiation of oligodendrocyte (OLG) progenitor cells (OPCs) into mature OLGs are key to understanding myelination and remyelination. Signaling via the retinoid X receptor γ (RXR-γ) has been shown be a positive regulator OPC differentiation. However, nuclear (NR) binding partner RXR-γ not established. In this study we show that binds several NRs in OPCs OLGs, one which is vitamin D (VDR). Using pharmacological knockdown approaches RXR-VDR signaling induces VDR...
Abstract Objective: Axon injury is a key contributor to the progression of disability in multiple sclerosis (MS). Systemic infections, which frequently precede relapses MS, have been linked clinical Alzheimer's disease. There evidence role for innate immune system MS lesions, as axonal associated with macrophage activation. We hypothesize that systemic inflammation leads enhanced damage consequence Methods: Monophasic experimental allergic encephalomyelitis (EAE) was induced cohort Lewis...
The role of the neurovascular niche in CNS myelin regeneration is incompletely understood. Here, we show that, upon demyelination, CNS-resident pericytes (PCs) proliferate, and parenchymal non-vessel-associated PC-like cells (PLCs) rapidly develop. During remyelination, mature oligodendrocytes were found close proximity to PCs. In Pdgfbret/ret mice, which have reduced PC numbers, oligodendrocyte progenitor cell (OPC) differentiation was delayed, although remyelination proceeded completion....
In brain inflammatory diseases, axonal damage is one of the most critical steps in cascade that leads to permanent disability. Thus, identifying initial events triggered by inflammation or oxidative stress provoke for development neuroprotective therapies. Energy depletion due mitochondrial dysfunction has been postulated as an important step axons. This prompted us study effects acute and on morphology, transport, function mitochondria axons.Mouse cerebellar slice cultures were challenged...
Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) that leads to severe neurological deficits. Due their immunomodulatory and neuroprotective activities ability promote generation oligodendrocytes, mesenchymal stem cells (MSCs) are currently being developed for autologous cell therapy in MS. As aging reduces regenerative capacity all tissues, it relevance investigate whether MSCs retain pro-oligodendrogenic activity with increasing age. We demonstrate...
Methylthioadenosine is a metabolite of the polyamine pathway that modulates methyltransferase activity, thereby influencing DNA and protein methylation. Since methylthioadenosine produces neuroprotection in models inflammation, ischemia epilepsy, we set out to evaluate role promoting remyelination, process will protect axons demyelinating diseases aid functional recovery. The effect remyelination was tested mouse cerebellum organotypic cultures were exposed lipopolysaccharide induce...
From 5th European Workshop on Immune-Mediated Inflammatory Diseases (Sitges-Barcelona, Spain. 1-3 December 2010)
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