María Asunción Barreda-Manso

ORCID: 0000-0003-4127-2101
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Research Areas
  • MicroRNA in disease regulation
  • RNA Interference and Gene Delivery
  • Circular RNAs in diseases
  • Nerve injury and regeneration
  • Spinal Cord Injury Research
  • Drug Transport and Resistance Mechanisms
  • Sphingolipid Metabolism and Signaling
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Endoplasmic Reticulum Stress and Disease
  • Neurogenesis and neuroplasticity mechanisms
  • Signaling Pathways in Disease
  • Glycosylation and Glycoproteins Research
  • Cell death mechanisms and regulation
  • Immune Response and Inflammation
  • Tryptophan and brain disorders
  • Lipid metabolism and biosynthesis
  • Bone fractures and treatments
  • NF-κB Signaling Pathways
  • Spine and Intervertebral Disc Pathology
  • Hereditary Neurological Disorders
  • Neonatal and fetal brain pathology
  • Cannabis and Cannabinoid Research
  • Neuroscience and Neuropharmacology Research
  • Nerve Injury and Rehabilitation

Hospital Nacional de Parapléjicos
2011-2025

Servicio de Salud de Castilla La Mancha
2011-2025

University College London
2024

National Hospital for Neurology and Neurosurgery
2024

Hospital Universitario Fundación Alcorcón
2018

Universidad Francisco de Vitoria
2017

Instituto Cajal
2011-2016

Consejo Superior de Investigaciones Científicas
2015

Bile acids are steroid found in the bile of mammals. The acid conjugate tauroursodeoxycholic (TUDCA) is neuroprotective different animal models stroke and neurological diseases. We have previously shown that TUDCA has anti‐inflammatory effects on glial cell cultures a mouse model acute neuroinflammation. show now microglial cells (central nervous system resident macrophages) express G protein‐coupled receptor 1/Takeda 5 (GPBAR1/TGR5) vivo vitro. binding to GPBAR1/TGR5 caused an increase...

10.1002/jcp.25742 article EN Journal of Cellular Physiology 2016-12-17

Because of their low levels expression and the inadequacy current research tools, CB2 cannabinoid receptors (CB2R) have been difficult to study, particularly in brain. This receptor is especially relevant context neuroinflammation, so novel tools are needed unveil its pathophysiological role(s). We generated a transgenic mouse model which enhanced green fluorescent protein (EGFP) under control cnr2 gene promoter through insertion an Internal Ribosomal Entry Site followed by EGFP coding...

10.1186/s12974-018-1174-9 article EN cc-by Journal of Neuroinflammation 2018-05-24

Bile acids are steroid found predominantly in the bile of mammals. The acid conjugate tauroursodeoxycholic (TUDCA) is a neuroprotective agent different animal models stroke and neurological diseases. However, anti-inflammatory properties TUDCA central nervous system (CNS) remain unknown. acute neuroinflammation model intracerebroventricular (icv) injection with bacterial lipopolysaccharide (LPS) C57BL/6 adult mice was used herein. Immunoreactivity against Iba-1, GFAP, VCAM-1 measured coronal...

10.1186/1742-2094-11-50 article EN cc-by Journal of Neuroinflammation 2014-03-19

Neuronal death is a central event in spinal cord injury (SCI) pathophysiology. Despite its importance, we have fragmentary vision of the process. In our opinion, research community has accumulated enough information to provide more detailed, integrated neuronal after SCI. This work embeds this by creating an open repository store and share data results from their analysis. We employed upload raw images sections mouse model contusive SCI used compare manual-, threshold-, neural network-based...

10.3390/ijms26083749 article EN International Journal of Molecular Sciences 2025-04-16

Mechanical trauma to the spinal cord causes extensive neuronal death, contributing loss of sensory-motor and autonomic functions below injury location. Apoptosis affects neurons after (SCI) is associated with increased caspase activity. Cleavage X-linked inhibitor apoptosis protein (XIAP) SCI may contribute this rise in Accordingly, we have shown that elevation XIAP resulted survival improved functional recovery. Therefore, hypothesise overexpression can be neuroprotective In line this,...

10.3390/ijms24032791 article EN International Journal of Molecular Sciences 2023-02-01

The synthesis and biological activity of oleylN-acetyl-α- β-d-glucosaminides (1 2, respectively) their thioglycosyl analogues (3 4, are reported. compounds exhibited antimitotic on rat glioma (C6) human lung carcinoma (A549) cell cultures in the micromolar range. Analysis extracts using ultra performance liquid chromatography-mass spectrometry showed that synthetic glycosides produce alterations glycosphingolipid metabolism, with variable effect level glucosylceramide depending configuration...

10.1021/jm200961q article EN HAL (Le Centre pour la Communication Scientifique Directe) 2011-10-13

COVID-19 pandemic is caused by betacoronavirus SARS-CoV-2. The genome of this virus composed a single strand RNA with 5' and 3'-UTR flanking region protein-coding ORFs closely resembling cells' mRNAs. MicroRNAs are endogenous post-transcriptional regulators that target mRNA to modulate protein expression mediate cellular functions, including antiviral defense. In the present study, we carried out bioinformatics screening search for human microRNAs targeting Results from computational...

10.3390/ijms22116094 article EN International Journal of Molecular Sciences 2021-06-05

The central nervous system microRNA miR-138-5p has attracted much attention in cancer research because it inhibits pro-apoptotic genes including CASP3. We hypothesize that downregulation after SCI leads to overexpression of genes, sensitizing neural cells noxious stimuli. This study aimed identify targets among overexpressed following and confirm modulates cell death cells. Gene expression histological analyses revealed the drop is due massive loss neurons oligodendrocytes its neurons....

10.3390/biomedicines10071559 article EN cc-by Biomedicines 2022-06-30

Following a central nervous system (CNS) injury, restoration of the blood-brain barrier (BBB) integrity is essential for recovering homeostasis. When this process delayed or impeded, blood substances and cells enter CNS parenchyma, initiating an additional inflammatory that extends initial injury causes so-called secondary neuronal loss. Astrocytes profibrotic mesenchymal react to migrate lesion site, creating new glia limitans restores BBB. This beneficial resolution inflammation, survival,...

10.1002/jcp.25655 article EN Journal of Cellular Physiology 2016-10-18

Central nervous system (CNS) injuries caused by cerebrovascular pathologies (e.g., stroke) or mechanical contusions traumatic brain injury) disrupt the blood-brain barrier (BBB) that protects CNS microenvironment from a direct contact with blood substances and cells. The initial neural damage trauma ischemic process is extended in time secondary neuronal loss due to reactive microglial cells leukocytes migrate lesion site produce inflammatory mediators oxygen species) increase cell death....

10.4103/1673-5374.169619 article EN cc-by-nc-sa Neural Regeneration Research 2015-01-01

Nogo-A protein is a key myelin-associated inhibitor of axonal growth, regeneration, and plasticity in the central nervous system (CNS). Regulation Nogo-A/NgR1 pathway facilitates functional recovery neural repair after spinal cord trauma ischemic stroke. MicroRNAs are described as effective tools for regulation important processes CNS, such neuronal differentiation, neuritogenesis, plasticity. Our results show that miR-182-5p mimic specifically downregulates expression luciferase reporter...

10.3390/ph15050529 article EN cc-by Pharmaceuticals 2022-04-25

ABSTRACT Spinal cord injury (SCI) is a disabling disorder of the spinal resulting from trauma or disease. Neuronal death central event in pathophysiology injury. Despite its importance and large number research studies carried out, we only have fragmentary vision process focused on specific targets each study. It our opinion that community has accumulated enough information which may be reanalyzed with novel tools to get much more detailed, integrated neuronal after SCI. This work embeds...

10.1101/2024.01.22.576608 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-01-23

Spinal cord injury (SCI) results in a cascade of primary and secondary damage, with apoptosis being prominent cause neuronal cell death. The X-linked inhibitor (XIAP) plays critical role inhibiting apoptosis, but its expression is reduced following SCI, contributing to increased vulnerability. This study investigates the regulatory miR-199a-5p on XIAP context SCI. Using bioinformatic tools, luciferase reporter assays, vitro vivo models we identified as post-transcriptional regulator XIAP....

10.3390/ijms252212374 article EN International Journal of Molecular Sciences 2024-11-18

Altered expression of microRNAs (miRNAs) after spinal cord injury (SCI) has been described as being responsible for the main secondary responses, such apoptosis. X-linked inhibitor apoptosis protein (XIAP) is a key apoptotic component involved in progression programmed cell death. Several regulators have to modulate XIAP's function, including post-transcriptional regulator's miRNAs. The aim present work identify miRNAs with altered SCI which can regulate XIAP expression. Our bioinformatic...

10.20944/preprints202212.0020.v2 preprint EN 2023-01-11

Neuronal maturation is a process that plays key role in the development and regeneration of central nervous system. Although embryonic brain neurodegeneration have received considerable attention, events govern postnatal neuronal are less understood. Among mechanisms influencing such processes, apoptosis role. Several regulators been described to modulate apoptosis, including post-transcriptional regulation by microRNAs. This study aimed analyze endogenous expression changes miR-138-5p, as...

10.3390/ijms242216509 article EN International Journal of Molecular Sciences 2023-11-20

ABSTRACT Spinal cord injury (SCI) is a major cause of permanent disability and its causes pathophysiological effects are very variables between patients. The assessment tissue damage extent neurodegeneration degree correlated with the functional evaluation most accepted tools to diagnose prognose trauma severity. Animal models SCI have been used for treatment development in present work we evaluate potency stereological estimate diagnostic neural degeneration locomotor sensorial after...

10.1101/2022.05.05.490720 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-05-05

Abstract Nogo-A protein is a key myelin-associated inhibitor for axonal growth, regeneration, and plasticity in the central nervous system (CNS). Regulation of Nogo-A/NgR1 pathway facilitates functional recovery neural repair after spinal cord trauma ischemic stroke. MicroRNAs are described as effective tools regulation important processes CNS such neuronal differentiation, neuritogenesis, plasticity. Our results showed that miR-182-5p mimic specifically downregulates expression luciferase...

10.1101/2022.03.03.482803 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2022-03-04

Trauma to the spinal cord causes extensive neuronal death contributing loss of sensory-motor and autonomic functions below injury level. Apoptosis affects neurons after (SCI) is associated with increased caspase activity. Cleavage X-linked inhibitor apoptosis protein (XIAP) SCI may contribute this rise Accordingly, we have shown that elevation XIAP resulted in survival improved functional recovery. Therefore, hypothesize overexpression can be neuroprotective In line this, studies a...

10.20944/preprints202212.0023.v1 preprint EN 2022-12-01

Altered expression of microRNAs (miRNAs) after spinal cord injury (SCI) has been described as being responsible for the main secondary responses, such apoptosis. X-linked inhibitor apoptosis protein (XIAP) is a key apoptotic component involved in progression programmed cell death. Several regulators have to modulate XIAP's function, including post-transcriptional regulator's miRNAs. The aim present work identify miRNAs with altered SCI which can regulate XIAP using bioinformatics and...

10.20944/preprints202212.0020.v1 preprint EN 2022-12-01
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