A5091191421- Nerve injury and regeneration
- Neurogenesis and neuroplasticity mechanisms
- Signaling Pathways in Disease
- Spinal Cord Injury Research
- Histone Deacetylase Inhibitors Research
- Axon Guidance and Neuronal Signaling
- Neuroinflammation and Neurodegeneration Mechanisms
- Cancer-related Molecular Pathways
- Neuroscience and Neuropharmacology Research
- Hereditary Neurological Disorders
- Cardiovascular and Diving-Related Complications
- Obstructive Sleep Apnea Research
- Genetics and Neurodevelopmental Disorders
- Diabetes Management and Research
- RNA Research and Splicing
- Nuclear Receptors and Signaling
- Neuroscience of respiration and sleep
- Genetic Neurodegenerative Diseases
- Genomics and Chromatin Dynamics
- Adipose Tissue and Metabolism
- Extracellular vesicles in disease
- Medicinal Plants and Bioactive Compounds
- Sleep and Wakefulness Research
- Regulation of Appetite and Obesity
- Head and Neck Surgical Oncology
Imperial College London
2015-2025
Campus Bio Medico University Hospital
2023-2025
Università Campus Bio-Medico
2023-2025
Hammersmith Hospital
2014-2024
Hertie Institute for Clinical Brain Research
2011-2021
University of Tübingen
2006-2020
University of Chieti-Pescara
2013-2017
Casa Sollievo della Sofferenza
2015
Neurology, Inc
2011
Center for Neuro-Oncology
2009
Traumatic brain injury (TBI) causes neuronal apoptosis, inflammation, and reactive astrogliosis, which contribute to secondary tissue loss, impaired regeneration, associated functional disabilities. Here, we show that up-regulation of cell cycle components is with caspase-mediated apoptosis glial proliferation after TBI in rats. In primary astrocyte cultures, inhibition (including the cyclin-dependent kinase inhibitors flavopiridol, roscovitine, olomoucine) reduced proteins, limited death...
Abstract Spinal cord injury causes secondary biochemical changes leading to neuronal cell death. To clarify the molecular basis of this delayed injury, we subjected rats spinal and identified gene expression patterns by high‐density oligonucleotide arrays (8,800 genes studied) at 30 minutes, 4 hours, 24 or 7 days after (total 26 U34A profiles). Detailed analyses were limited 4,300 consistently expressed above background. Temporal clustering showed rapid immediate early (30 minutes), followed...
The activity of the p53 gene product is regulated by a plethora posttranslational modifications. An open question whether such changes act redundantly or dependently upon one another. We show that functional interference between specific acetylated and phosphorylated residues influences cell fate. Acetylation lysine 320 (K320) prevents phosphorylation crucial serines in NH2-terminal region p53; only allows activation genes containing high-affinity binding sites, as p21/WAF; promotes survival...
Spinal cord injury (SCI) causes delayed secondary biochemical alterations that lead to tissue loss and associated neurological dysfunction. Up-regulation of cell cycle proteins occurs in both neurons glia after SCI may contribute these changes. The present study examined the role activation on severe rat. caused protein up-regulation with neuronal oligodendroglial apoptosis, glial scar formation microglial activation. Treatment inhibitor flavopiridol reduced induction significantly improved...
Axonal regeneration and related functional recovery following axonal injury in the adult central nervous system are extremely limited, due to a lack of neuronal intrinsic competence presence extrinsic inhibitory signals. As opposed what occurs during development, weak proregenerative gene expression programme contributes limited capacity injured axons regenerate. Here we show, an optic nerve crush model injury, that adenoviral (cytomegalovirus promoter) overexpression acetyltransferase p300,...
After a spinal cord injury, axons fail to regenerate in the adult mammalian central nervous system, leading permanent deficits sensory and motor functions. Increasing neuronal activity after an injury using electrical stimulation or rehabilitation can enhance plasticity result some degree of recovery; however, underlying mechanisms remain poorly understood. We found that placing mice enriched environment before enhanced proprioceptive dorsal root ganglion neurons, lasting increase their...
Aging is associated with increased prevalence of axonal injuries characterized by poor regeneration and disability. However, the underlying mechanisms remain unclear. In our experiments, RNA sequencing sciatic dorsal root ganglia (DRG) revealed significant aging-dependent enrichment in T cell signaling both before after nerve injury (SNI) mice. Lymphotoxin activated transcription factor NF-κB, which induced expression chemokine CXCL13 neurons. This turn recruited CXCR5
Spinal cord injury (SCI) increasingly affects aged individuals, where functional impairment and mortality are highest. However, the aging-dependent mechanisms underpinning tissue damage remain elusive. Here, we find that natural killer-like T (NKLT) cells seed intact human murine spinal multiply further after injury. NKLT accumulate in via C-X-C motif chemokine receptor 6 ligand 16 signaling to clonally expand by engaging with major histocompatibility complex (MHC)-I-expressing myeloid...
Purpose.: Valproic acid (VPA) has been demonstrated to have neuroprotective effects in neurodegenerative conditions. VPA inhibits histone-deacetylases (HDAC) and delays apoptosis degenerating neurons. The authors investigated whether retinal ganglion cell (RGC) death enhances axonal regeneration after optic nerve crush (ONC). Furthermore, potential molecular targets involved VPA-mediated protection were analyzed. Methods.: ONC was performed on the left eye of rats, which received or Ringer's...
HDAC3 inhibition has been shown to improve memory and reduce amyloid-β (Aβ) in Alzheimer's disease (AD) models, but the underlying mechanisms are unclear. We investigated molecular effects of on AD pathology, using vitro ex vivo models AD, based our finding that expression is increased brains. For this purpose, N2a mouse neuroblastoma cells as well organotypic brain cultures (OBCSs) 5XFAD wild-type mice were incubated with various concentrations selective inhibitor RGFP966 (0.1-10 μM) for 24...
AbstractUp-regulation of cell cycle proteins occurs in both mitotic and post-mitotic neural cells after central nervous system (CNS) injury adult animals. In cells, such as astroglia microglia, they induce proliferation, whereas neurons initiate caspase-related apoptosis. We recently reported that early administration the inhibitor flavopiridol experimental traumatic brain (TBI) significantly reduced lesion volume, scar formation neuronal death, while promoting near complete behavioral...
Changes in gene expression contribute to pathophysiological alterations following spinal cord injury (SCI). We examined over time (4 h, 24 7 days) at the impact site, as well rostral and caudal regions, mild, moderate, or severe contusion SCI rats. High-density oligonucleotide microarrays were used that included approximately 27,000 genes/ESTs (Affymetrix RG-U34; A, B C arrays), together with multiple analyses (MAS 5.0, dChip). Alterations after mild relatively rapid h), whereas they delayed...
Following spinal cord injury, there are numerous changes in gene expression that appear to contribute either neurodegeneration or reparative processes. We utilized high density oligonucleotide microarrays examine temporal profile after injury rats with the goal of identifying novel factors involved neural plasticity. By comparing mRNA were coordinately regulated over time genes previously implicated nerve regeneration plasticity, we found a cluster whose members cell adhesion processes,...
Regeneration of injured central nervous system axons is highly restricted, causing neurological impairment. To date, although the lack intrinsic regenerative potential well described, a key regulatory molecular mechanism for enhancement both axonal regrowth and functional recovery after injury remains elusive. While ubiquitin ligases coordinate neuronal morphogenesis connectivity during development as injury, their role specifically in regeneration unknown. Following bioinformatics network...
Physiological levels of ROS support neurite outgrowth and axonal specification, but the mechanisms by which are able to shape neurons remain unknown. Ca 2+ , a broad intracellular second messenger, promotes both Rac1 activation extension. release from endoplasmic reticulum, mediated IP3R1 ryanodine receptor (RyR) channels, requires physiological that mainly sustained NADPH oxidase (NOX) complex. In this work, we explore contribution link between NOX RyR-mediated toward specification rat...