A5101463780- Pain Mechanisms and Treatments
- Cancer-related cognitive impairment studies
- Adenosine and Purinergic Signaling
- Brain Metastases and Treatment
- Sphingolipid Metabolism and Signaling
- Nerve injury and regeneration
- Pharmacological Receptor Mechanisms and Effects
- Stress Responses and Cortisol
- Histone Deacetylase Inhibitors Research
- Apelin-related biomedical research
- Sleep and Wakefulness Research
- Circadian rhythm and melatonin
- Immune Response and Inflammation
- Neuroinflammation and Neurodegeneration Mechanisms
- Neuroscience and Neuropharmacology Research
- Neuropeptides and Animal Physiology
- Alzheimer's disease research and treatments
- Macrophage Migration Inhibitory Factor
- Ion Channels and Receptors
- Neurogenesis and neuroplasticity mechanisms
- Adipose Tissue and Metabolism
- Advanced Breast Cancer Therapies
- Hypothalamic control of reproductive hormones
- Gastrointestinal motility and disorders
- Dermatology and Skin Diseases
Saint Louis University
2017-2022
Czech Academy of Sciences, Institute of Physiology
2022
Sapienza University of Rome
2019-2021
Significance Understanding the cellular and molecular pathways of neuropathic pain is fundamental to discovering classes non-opioid analgesics. Emerging evidence implicates altered sphingolipid metabolism elevated levels sphingosine-1-phosphate (S1P) in spinal cord persistence pain, but its neuropharmacology engaged are poorly understood. Using a multidisciplinary approach, we provide that S1P drives by selectively activating receptor subtype 1 (S1PR1) astrocytes. Inhibiting S1PR1 attenuated...
The A3 adenosine receptor (A3AR) has emerged as a therapeutic target with A3AR agonists to tackle the global challenge of neuropathic pain, and investigation into its mode action is essential for ongoing clinical development. Immune cell A3ARs, their activation during pathology, modulate cytokine release. Thus, use immune cells cellular substrate pharmacological enticing, but unknown. present study discovered that Rag-KO mice lacking T B cells, compared WT mice, are insensitive...
Cisplatin is used to combat solid tumors. However, patients treated with cisplatin often develop cognitive impairments, sensorimotor deficits, and peripheral neuropathy. There no FDA-approved treatment for these neurotoxicities. We investigated the capacity of a highly selective A3 adenosine receptor (AR) subtype (A3AR) agonist, MRS5980, prevent reverse cisplatin-induced MRS5980 prevented impairment (decreased executive function impaired spatial working memory), neuropathic pain (mechanical...
Cancer-related cognitive impairment (CRCI) is a major neurotoxicity affecting more than 50% of cancer survivors. The underpinning mechanisms are mostly unknown, and there no FDA-approved interventions. Sphingolipidomic analysis mouse prefrontal cortex hippocampus, key sites function, revealed that cisplatin increased levels the potent signaling molecule sphingosine-1-phosphate (S1P) led to impairment. At biochemical level, S1P induced mitochondrial dysfunction, activation NOD-, LRR-, pyrin...
Chemotherapy-induced peripheral neuropathy accompanied by neuropathic pain (CIPN) is a major neurotoxicity of cisplatin, platinum-based drug widely used for lung, ovarian, and testicular cancer treatment. CIPN causes discontinuation severely impacts life quality with no FDA-approved interventions. We previously reported that drugs increase levels sphingosine 1-phosphate (S1P) in the spinal cord drive through activating S1P receptor subtype 1 (S1PR1). However, mechanisms engaged downstream...
Acute inflammation is particularly relevant in the pathogenesis of visceral hypersensitivity associated with inflammatory bowel diseases. Glia within enteric nervous system, as well central contributes to neuroplasticity during inflammation, but whether glia has potential modify sensitivity following colitis still unknown. This work aimed investigate occurrence changes neuron-glial networks controlling perception along gut-brain axis colitis, and assess effects peripheral glial manipulation....
The secreted bioactive peptide prokineticin 2 (PK2) is a potent adipokine and its central peripheral administration reduces food intake in rodents. pk2 gene has two splice variants, PK2 PK2L (PK2 long form), which cleaved into an active peptide, PK2β, that preferentially binds receptor 1 (PKR1). We investigated the role of PK2β regulation intake. demonstrated intraperitoneal injection contrast to PK2, did not reduce mice. Exposure hypotalamic explants but induced phosphorylation STAT3 ERK....
Department of Pharmacology and Physiology, Henry Amelia Nasrallah Center for Neuroscience, Saint Louis University School Medicine, St. Louis, MO, United States *Corresponding author. Address: Schwitalla Hall 1402 S. Grand Blvd, MO 63104, States. Tel.: 314-977-6430. E-mail address: [email protected] (D. Salvemini). Sponsorships or competing interests that may be relevant to content are disclosed at the end this article.
<b>Abstract ID 20618</b> <b>Poster Board 400</b> Paclitaxel, standard-of-care first-line chemotherapy for epithelial ovarian cancer and triple negative breast cancer, was shown to impair learning memory functions in >50% of survivors. Underpinning mechanisms this major neurotoxicity are still mostly unknown, there no FDA-approved interventions. We developed a mouse model paclitaxel-induced cognitive impairment whose cumulative dose is comparable the total per cycle used patients....
<b>Abstract ID 56337</b> <b>Poster Board 352</b> Chemotherapy-induced peripheral neuropathy accompanied by neuropathic pain (CINP) is a major neurotoxicity of cisplatin, which platinum-based drug widely used for the treatment lung, ovarian, and testicular cancer. CINP causes discontinuation severely impacts quality life; there are no FDA-approved interventions. We have reported that drugs increase levels sphingolipid, sphingosine 1-phosphate (S1P) in spinal cord drive through activation S1P...