A5071570104- Pain Mechanisms and Treatments
- Neuroscience and Neuropharmacology Research
- Nerve injury and regeneration
- Botulinum Toxin and Related Neurological Disorders
- Musculoskeletal pain and rehabilitation
- Pediatric Pain Management Techniques
- Hereditary Neurological Disorders
- Single-cell and spatial transcriptomics
- Pain Management and Placebo Effect
- Cancer, Stress, Anesthesia, and Immune Response
- Cancer-related molecular mechanisms research
- Cancer Treatment and Pharmacology
- Histone Deacetylase Inhibitors Research
- MicroRNA in disease regulation
- Ion channel regulation and function
- Epigenetics and DNA Methylation
- Sexual function and dysfunction studies
- Neurological Disease Mechanisms and Treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Fibromyalgia and Chronic Fatigue Syndrome Research
- Neuropeptides and Animal Physiology
- Pharmacological Effects and Toxicity Studies
Chinese University of Hong Kong
2023
Heidelberg University
2011-2022
University Hospital Heidelberg
2013-2015
European Molecular Biology Laboratory
2013
Abstract Mechanisms underlying central neuropathic pain are poorly understood. Although glial dysfunction has been functionally linked with pain, very little is known about modulation of by oligodendrocytes. Here we report that genetic ablation oligodendrocytes rapidly triggers a pattern sensory changes closely resemble which manifest before overt demyelination. Primary oligodendrocyte loss not associated autoreactive T- and B-cell infiltration in the spinal cord neither activation microglia...
Abstract Background Pain can be one of the most severe symptoms associated with multiple sclerosis (MS) and develops varying levels time courses. MS-related pain is difficult to treat, since very little known about mechanisms underlying its development. Animal models experimental autoimmune encephalomyelitis (EAE) mimic many aspects MS are well-suited study pathophysiological mechanisms. Yet, date sensory abnormalities in different EAE models. We therefore aimed thoroughly characterize...
Abstract Synaptic plasticity is the cornerstone of processes underlying persistent nociceptive activity-induced changes in normal sensitivity. Kalirin-7 a multifunctional guanine-nucleotide-exchange factor (GEF) for Rho GTPases that characterized by its localization at excitatory synapses, interactions with glutamate receptors and ability to dynamically modulate neuronal cytoskeleton. Here we show spinally expressed required activity-dependent synaptic long-term potentiation as well...
Pathophysiological mechanisms underlying pain associated with cancer are poorly understood. microRNAs (miRNAs) a class of noncoding RNAs emerging functional importance in chronic pain. In genome-wide screen for miRNAs regulated dorsal root ganglia (DRG) neurons mouse model bone metastatic pain, we identified miR-34c-5p as functionally important pronociceptive miRNA. Despite these insights and therapeutic potential miR-34c-5p, its molecular mechanism action peripheral sensory remains unknown....
Abstract Persistent pain is sustained by maladaptive changes in gene transcription resulting altered function of the relevant circuits; therapies are still unsatisfactory. The epigenetic mechanisms and affected genes linking nociceptive activity to transcriptional pathological sensitivity unclear. Here, we found that, among several histone deacetylases (HDACs), synaptic specifically affects HDAC4 murine spinal cord dorsal horn neurons. Noxious stimuli that induce long-lasting inflammatory...
Chronic pain is a pathological manifestation of neuronal plasticity supported by altered gene transcription in spinal cord neurons that results long-lasting hypersensitivity. Recently, the concept epigenetic regulators might be important has emerged, but clear understanding molecular players involved process still lacking. In this study, we linked Dnmt3a2, synaptic activity-regulated de novo DNA methyltransferase, to chronic inflammatory pain. We observed Dnmt3a2 levels are increased adult...