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Article ; Online: Sex-differences in prostaglandin signaling: a semi-systematic review and characterization of PTGDS expression in human sensory neurons.

Shen, Breanna Q / Sankaranarayanan, Ishwarya / Price, Theodore J / Tavares-Ferreira, Diana

2023 Volume 13, Issue 1, Page(s) 4670

Abstract: There is increasing evidence of sex differences in underlying mechanisms causing pain in preclinical models, and in clinical populations. There are also important disconnects between clinical pain populations and the way preclinical pain studies are ... ...

Abstract	There is increasing evidence of sex differences in underlying mechanisms causing pain in preclinical models, and in clinical populations. There are also important disconnects between clinical pain populations and the way preclinical pain studies are conducted. For instance, osteoarthritis pain more frequently affects women, but most preclinical studies have been conducted using males in animal models. The most widely used painkillers, nonsteroidal anti-inflammatory drugs (NSAIDs), act on the prostaglandin pathway by inhibiting cyclooxygenase (COX) enzymes. The purpose of this study was to analyze the preclinical and clinical literature on the role of prostaglandins and COX in inflammation and pain. We aimed to specifically identify studies that used both sexes and investigate whether any sex-differences in the action of prostaglandins and COX inhibition had been reported, either in clinical or preclinical studies. We conducted a PubMed search and identified 369 preclinical studies and 100 clinical studies that matched our inclusion/exclusion criteria. Our analysis shows that only 17% of preclinical studies on prostaglandins used both sexes and, out of those, only 19% analyzed or reported data separated by sex. In contrast, 79% of the clinical studies analyzed used both sexes. However, only 6% of those reported data separated by sex. Interestingly, 14 out of 15 preclinical studies and 5 out of 6 clinical studies that analyzed data separated by sex have identified sex-differences. This builds on the increasing evidence of sex-differences in prostaglandin signaling and the importance of sex as a biological variable in data analysis. The preclinical literature identifies a sex difference in prostaglandin D
MeSH term(s)	Animals ; Female ; Humans ; Male ; Cyclooxygenase 2 ; Pain ; Prostaglandins/metabolism ; Sensory Receptor Cells/metabolism ; Sex Characteristics
Chemical Substances	Cyclooxygenase 2 (EC 1.14.99.1) ; Prostaglandins ; PTGDS protein, human (EC 5.3.-)
Language	English
Publishing date	2023-03-22
Publishing country	England
Document type	Systematic Review ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-31603-x
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Article ; Online: NOCICEPTRA2.0 - A comprehensive ncRNA atlas of human native and iPSC-derived sensory neurons.

Zeidler, Maximilian / Tavares-Ferreira, Diana / Brougher, Jackson / Price, Theodore J / Kress, Michaela

iScience

2023 Volume 26, Issue 12, Page(s) 108525

Abstract: Non-coding RNAs (ncRNAs) are pivotal in gene regulation during development and disease. MicroRNAs have been extensively studied in neurogenesis. However, limited knowledge exists about the developmental signatures of other ncRNA species in sensory neuron ...

Abstract	Non-coding RNAs (ncRNAs) are pivotal in gene regulation during development and disease. MicroRNAs have been extensively studied in neurogenesis. However, limited knowledge exists about the developmental signatures of other ncRNA species in sensory neuron differentiation, and human dorsal root ganglia (DRG) ncRNA expression remains undocumented. To address this gap, we generated a comprehensive atlas of small ncRNA species during iPSC-derived sensory neuron differentiation. Utilizing iPSC-derived sensory neurons and human DRG RNA sequencing, we unveiled signatures describing developmental processes. Our analysis identified ncRNAs associated with various sensory neuron stages. Striking similarities in ncRNA expression signatures between human DRG and iPSC-derived neurons support the latter as a model to bridge the translational gap between preclinical findings and human disorders. In summary, our research sheds light on the role of ncRNA species in human nociceptors, and NOCICEPTRA2.0 offers a comprehensive ncRNA database for sensory neurons that researchers can use to explore ncRNA regulators in nociceptors thoroughly.
Language	English
Publishing date	2023-11-23
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.108525
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Article ; Online: Inducible co-stimulatory molecule (ICOS) alleviates paclitaxel-induced neuropathic pain via an IL-10-mediated mechanism in female mice.

Sankaranarayanan, Ishwarya / Tavares-Ferreira, Diana / Mwirigi, Juliet M / Mejia, Galo L / Burton, Michael D / Price, Theodore J

Journal of neuroinflammation

2023 Volume 20, Issue 1, Page(s) 32

Abstract: Chemotherapy-induced peripheral neuropathy (CIPN) is a primary dose-limiting side effect caused by antineoplastic agents, such as paclitaxel. A primary symptom of this neuropathy is pain. Currently, there are no effective treatments for CIPN, which can ... ...

Abstract	Chemotherapy-induced peripheral neuropathy (CIPN) is a primary dose-limiting side effect caused by antineoplastic agents, such as paclitaxel. A primary symptom of this neuropathy is pain. Currently, there are no effective treatments for CIPN, which can lead to long-term morbidity in cancer patients and survivors. Neuro-immune interactions occur in CIPN pain and have been implicated both in the development and progression of pain in CIPN and the resolution of pain in CIPN. We investigated the potential role of inducible co-stimulatory molecule (ICOS) in the resolution of CIPN pain-like behaviors in mice. ICOS is an immune checkpoint molecule that is expressed on the surface of activated T cells and promotes proliferation and differentiation of T cells. We found that intrathecal administration of ICOS agonist antibody (ICOSaa) alleviates mechanical hypersensitivity caused by paclitaxel and facilitates the resolution of mechanical hypersensitivity in female mice. Administration of ICOSaa reduced astrogliosis in the spinal cord and satellite cell gliosis in the DRG of mice previously treated with paclitaxel. Mechanistically, ICOSaa intrathecal treatment promoted mechanical hypersensitivity resolution by increasing interleukin 10 (IL-10) expression in the dorsal root ganglion. In line with these observations, blocking IL-10 receptor (IL-10R) activity occluded the effects of ICOSaa treatment on mechanical hypersensitivity in female mice. Suggesting a broader activity in neuropathic pain, ICOSaa also partially resolved mechanical hypersensitivity in the spared nerve injury (SNI) model. Our findings support a model wherein ICOSaa administration induces IL-10 expression to facilitate neuropathic pain relief in female mice. ICOSaa treatment is in clinical development for solid tumors and given our observation of T cells in the human DRG, ICOSaa therapy could be developed for combination chemotherapy-CIPN clinical trials.
MeSH term(s)	Animals ; Female ; Humans ; Mice ; Antineoplastic Agents/pharmacology ; Ganglia, Spinal/metabolism ; Hyperalgesia/chemically induced ; Hyperalgesia/drug therapy ; Hyperalgesia/metabolism ; Inducible T-Cell Co-Stimulator Protein/metabolism ; Interleukin-10/metabolism ; Neuralgia/chemically induced ; Neuralgia/drug therapy ; Neuralgia/metabolism ; Paclitaxel/adverse effects
Chemical Substances	Antineoplastic Agents ; Icos protein, mouse ; Inducible T-Cell Co-Stimulator Protein ; Interleukin-10 (130068-27-8) ; Paclitaxel (P88XT4IS4D)
Language	English
Publishing date	2023-02-11
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-023-02719-8
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Article ; Online: Characterization of Fragile X Mental Retardation Protein expression in human nociceptors and their axonal projections to the spinal dorsal horn.

Mitchell, Molly E / Cook, Lauren C / Shiers, Stephanie / Tavares-Ferreira, Diana / Akopian, Armen N / Dussor, Gregory / Price, Theodore J

The Journal of comparative neurology

2023 Volume 531, Issue 7, Page(s) 814–835

Abstract: Fragile X Mental Retardation Protein (FMRP) regulates activity-dependent RNA localization and local translation to modulate synaptic plasticity throughout the central nervous system. Mutations in the FMR1 gene that hinder or ablate FMRP function cause ... ...

Abstract	Fragile X Mental Retardation Protein (FMRP) regulates activity-dependent RNA localization and local translation to modulate synaptic plasticity throughout the central nervous system. Mutations in the FMR1 gene that hinder or ablate FMRP function cause Fragile X Syndrome (FXS), a disorder associated with sensory processing dysfunction. FXS premutations are associated with increased FMRP expression and neurological impairments including sex dimorphic presentations of chronic pain. In mice, FMRP ablation causes dysregulated dorsal root ganglion (DRG) neuron excitability and synaptic vesicle exocytosis, spinal circuit activity, and decreased translation-dependent nociceptive sensitization. Activity-dependent, local translation is a key mechanism for enhancing primary nociceptor excitability that promotes pain in animals and humans. These works indicate that FMRP likely regulates nociception and pain at the level of the primary nociceptor or spinal cord. Therefore, we sought to better understand FMRP expression in the human DRG and spinal cord using immunostaining in organ donor tissues. We find that FMRP is highly expressed in DRG and spinal neuron subsets with substantia gelatinosa exhibiting the most abundant immunoreactivity in spinal synaptic fields. Here, it is expressed in nociceptor axons. FMRP puncta colocalized with Nav1.7 and TRPV1 receptor signals suggesting a pool of axoplasmic FMRP localizes to plasma membrane-associated loci in these branches. Interestingly, FMRP puncta exhibited notable colocalization with calcitonin gene-related peptide (CGRP) immunoreactivity selectively in female spinal cord. Our results support a regulatory role for FMRP in human nociceptor axons of the dorsal horn and implicate it in the sex dimorphic actions of CGRP signaling in nociceptive sensitization and chronic pain.
MeSH term(s)	Humans ; Animals ; Mice ; Female ; Fragile X Mental Retardation Protein/genetics ; Fragile X Mental Retardation Protein/metabolism ; Nociceptors/metabolism ; Chronic Pain ; Calcitonin Gene-Related Peptide/metabolism ; Axons/metabolism ; Fragile X Syndrome/genetics ; Spinal Cord Dorsal Horn/metabolism
Chemical Substances	Fragile X Mental Retardation Protein (139135-51-6) ; Calcitonin Gene-Related Peptide (JHB2QIZ69Z) ; FMR1 protein, human ; Fmr1 protein, mouse
Language	English
Publishing date	2023-02-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3086-7
ISSN	1096-9861 ; 0021-9967 ; 0092-7317
ISSN (online)	1096-9861
ISSN	0021-9967 ; 0092-7317
DOI	10.1002/cne.25463
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Article ; Online: 4E-BP1-dependent translation in nociceptors controls mechanical hypersensitivity via TRIM32/type I interferon signaling.

Wong, Calvin / Tavares-Ferreira, Diana / Thörn Perez, Carolina / Sharif, Behrang / Uttam, Sonali / Amiri, Mehdi / Lister, Kevin C / Hooshmandi, Mehdi / Nguyen, Vivienne / Séguéla, Philippe / Sonenberg, Nahum / Price, Theodore J / Gkogkas, Christos G / Khoutorsky, Arkady

Science advances

2023 Volume 9, Issue 44, Page(s) eadh9603

Abstract: Activation of the mechanistic target of rapamycin complex 1 (mTORC1) contributes to the development of chronic pain. However, the specific mechanisms by which mTORC1 causes hypersensitivity remain elusive. The eukaryotic initiation factor 4E-binding ... ...

Abstract	Activation of the mechanistic target of rapamycin complex 1 (mTORC1) contributes to the development of chronic pain. However, the specific mechanisms by which mTORC1 causes hypersensitivity remain elusive. The eukaryotic initiation factor 4E-binding protein 1 (4E-BP1) is a key mTORC1 downstream effector that represses translation initiation. Here, we show that nociceptor-specific deletion of 4E-BP1, mimicking activation of mTORC1-dependent translation, is sufficient to cause mechanical hypersensitivity. Using translating ribosome affinity purification in nociceptors lacking 4E-BP1, we identified a pronounced translational up-regulation of tripartite motif-containing protein 32 (TRIM32), an E3 ubiquitin ligase that promotes interferon signaling. Down-regulation of TRIM32 in nociceptors or blocking type I interferon signaling reversed the mechanical hypersensitivity in mice lacking 4E-BP1. Furthermore, nociceptor-specific ablation of TRIM32 alleviated mechanical hypersensitivity caused by tissue inflammation. These results show that mTORC1 in nociceptors promotes hypersensitivity via 4E-BP1-dependent up-regulation of TRIM32/interferon signaling and identify TRIM32 as a therapeutic target in inflammatory pain.
MeSH term(s)	Mice ; Animals ; Nociceptors/metabolism ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Cell Cycle Proteins/metabolism ; Phosphoproteins/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Interferon Type I/metabolism ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Cell Cycle Proteins ; Phosphoproteins ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Interferon Type I ; TRIM32 protein, mouse (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2023-11-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adh9603
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Article: Analysis of matrisome expression patterns in murine and human dorsal root ganglia.

Vroman, Robin / Hunter, Rahel S / Wood, Matthew J / Davis, Olivia C / Malfait, Zoë / George, Dale S / Ren, Dongjun / Tavares-Ferreira, Diana / Price, Theodore J / Miller, Richard J / Malfait, Anne-Marie / Malfait, Fransiska / Miller, Rachel E / Syx, Delfien

Frontiers in molecular neuroscience

2023 Volume 16, Page(s) 1232447

Abstract: The extracellular matrix (ECM) is a dynamic structure of molecules that can be divided into six different categories and are collectively called the matrisome. The ECM plays pivotal roles in physiological processes in many tissues, including the nervous ... ...

Abstract	The extracellular matrix (ECM) is a dynamic structure of molecules that can be divided into six different categories and are collectively called the matrisome. The ECM plays pivotal roles in physiological processes in many tissues, including the nervous system. Intriguingly, alterations in ECM molecules/pathways are associated with painful human conditions and murine pain models. Nevertheless, mechanistic insight into the interplay of normal or defective ECM and pain is largely lacking. The goal of this study was to integrate bulk, single-cell, and spatial RNA sequencing (RNAseq) datasets to investigate the expression and cellular origin of matrisome genes in male and female murine and human dorsal root ganglia (DRG). Bulk RNAseq showed that about 65% of all matrisome genes were expressed in both murine and human DRG, with proportionally more core matrisome genes (glycoproteins, collagens, and proteoglycans) expressed compared to matrisome-associated genes (ECM-affiliated genes, ECM regulators, and secreted factors). Single cell RNAseq on male murine DRG revealed the cellular origin of matrisome expression. Core matrisome genes, especially collagens, were expressed by fibroblasts whereas matrisome-associated genes were primarily expressed by neurons. Cell-cell communication network analysis with CellChat software predicted an important role for collagen signaling pathways in connecting vascular cell types and nociceptors in murine tissue, which we confirmed by analysis of spatial transcriptomic data from human DRG. RNAscope
Language	English
Publishing date	2023-08-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2023.1232447
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Article ; Online: Fibroblast-derived PI16 sustains inflammatory pain via regulation of CD206

Garrity, Rachelle / Arora, Neha / Haque, Md Areeful / Weis, Drew / Trinh, Ronnie T / Neerukonda, Sanjay V / Kumari, Susmita / Cortez, Ibdanelo / Ubogu, Eroboghene E / Mahalingam, Rajasekaran / Tavares-Ferreira, Diana / Price, Theodore J / Kavelaars, Annemieke / Heijnen, Cobi J / Shepherd, Andrew J

Brain, behavior, and immunity

2023 Volume 112, Page(s) 220–234

Abstract: Originally identified in fibroblasts, Protease Inhibitor (PI)16 was recently shown to be crucial for the development of neuropathic pain via effects on blood-nerve barrier permeability and leukocyte infiltration, though its impact on inflammatory pain ... ...

Abstract	Originally identified in fibroblasts, Protease Inhibitor (PI)16 was recently shown to be crucial for the development of neuropathic pain via effects on blood-nerve barrier permeability and leukocyte infiltration, though its impact on inflammatory pain has not been established. Using the complete Freund's Adjuvant inflammatory pain model, we show that Pi16
MeSH term(s)	Mice ; Humans ; Animals ; Chronic Pain ; Neuralgia ; Inflammation ; Macrophages ; Fibroblasts ; Antibodies, Neutralizing/pharmacology ; Ganglia, Spinal ; Hyperalgesia ; Carrier Proteins ; Glycoproteins
Chemical Substances	Antibodies, Neutralizing ; PI16 protein, human ; Carrier Proteins ; Glycoproteins
Language	English
Publishing date	2023-06-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2023.06.011
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Zs.A 2276: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: RNA profiling of human dorsal root ganglia reveals sex differences in mechanisms promoting neuropathic pain.

Ray, Pradipta R / Shiers, Stephanie / Caruso, James P / Tavares-Ferreira, Diana / Sankaranarayanan, Ishwarya / Uhelski, Megan L / Li, Yan / North, Robert Y / Tatsui, Claudio / Dussor, Gregory / Burton, Michael D / Dougherty, Patrick M / Price, Theodore J

Brain : a journal of neurology

2022 Volume 146, Issue 2, Page(s) 749–766

Abstract: Neuropathic pain is a leading cause of high-impact pain, is often disabling and is poorly managed by current therapeutics. Here we focused on a unique group of neuropathic pain patients undergoing thoracic vertebrectomy where the dorsal root ganglia is ... ...

Abstract	Neuropathic pain is a leading cause of high-impact pain, is often disabling and is poorly managed by current therapeutics. Here we focused on a unique group of neuropathic pain patients undergoing thoracic vertebrectomy where the dorsal root ganglia is removed as part of the surgery allowing for molecular characterization and identification of mechanistic drivers of neuropathic pain independently of preclinical models. Our goal was to quantify whole transcriptome RNA abundances using RNA-seq in pain-associated human dorsal root ganglia from these patients, allowing comprehensive identification of molecular changes in these samples by contrasting them with non-pain-associated dorsal root ganglia. We sequenced 70 human dorsal root ganglia, and among these 50 met inclusion criteria for sufficient neuronal mRNA signal for downstream analysis. Our expression analysis revealed profound sex differences in differentially expressed genes including increase of IL1B, TNF, CXCL14 and OSM in male and CCL1, CCL21, PENK and TLR3 in female dorsal root ganglia associated with neuropathic pain. Coexpression modules revealed enrichment in members of JUN-FOS signalling in males and centromere protein coding genes in females. Neuro-immune signalling pathways revealed distinct cytokine signalling pathways associated with neuropathic pain in males (OSM, LIF, SOCS1) and females (CCL1, CCL19, CCL21). We validated cellular expression profiles of a subset of these findings using RNAscope in situ hybridization. Our findings give direct support for sex differences in underlying mechanisms of neuropathic pain in patient populations.
MeSH term(s)	Female ; Humans ; Male ; Ganglia, Spinal/metabolism ; Neuralgia/genetics ; Neuralgia/metabolism ; RNA/metabolism ; Transcriptome ; Sex Factors
Chemical Substances	RNA (63231-63-0)
Language	English
Publishing date	2022-07-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awac266
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Article ; Online: Meteorin Alleviates Paclitaxel-Induced Peripheral Neuropathic Pain in Mice.

Sankaranarayanan, Ishwarya / Tavares-Ferreira, Diana / He, Lucy / Kume, Moeno / Mwirigi, Juliet M / Madsen, Torsten M / Petersen, Kenneth A / Munro, Gordon / Price, Theodore J

The journal of pain

2022 Volume 24, Issue 4, Page(s) 555–567

Abstract: Chemotherapy-induced peripheral neuropathy is a challenging condition to treat, and arises due to severe, dose-limiting toxicity of chemotherapeutic drugs such as paclitaxel. This often results in debilitating sensory and motor deficits that are not ... ...

Abstract	Chemotherapy-induced peripheral neuropathy is a challenging condition to treat, and arises due to severe, dose-limiting toxicity of chemotherapeutic drugs such as paclitaxel. This often results in debilitating sensory and motor deficits that are not effectively prevented or alleviated by existing therapeutic interventions. Recent studies have demonstrated the therapeutic effects of Meteorin, a neurotrophic factor, in reversing neuropathic pain in rodent models of peripheral nerve injury induced by physical trauma. Here, we sought to investigate the potential antinociceptive effects of recombinant mouse Meteorin (rmMeteorin) using a paclitaxel-induced peripheral neuropathy model in male and female mice. Paclitaxel treatment (4 × 4 mg/kg, i.p.) induced hind paw mechanical hypersensitivity by day 8 after treatment. Thereafter, in a reversal dosing paradigm, five repeated injections of rmMeteorin (.5 and 1.8 mg/kg s.c. respectively) administered over 9 days produced a significant and long-lasting attenuation of mechanical hypersensitivity in both sexes. Additionally, administration of rmMeteorin ( .5 and 1.8 mg/kg), initiated before and during paclitaxel treatment (prevention dosing paradigm), reduced the establishment of hind paw mechanical hypersensitivity. Repeated systemic administration of rmMeteorin in both dosing paradigms decreased histochemical signs of satellite glial cell reactivity as measured by glutamine synthetase and connexin 43 protein expression in the dorsal root ganglion. Additionally, in the prevention administration paradigm rmMeteorin had a protective effect against paclitaxel-induced loss of intraepidermal nerve fibers. Our findings indicate that rmMeteorin has a robust and sustained antinociceptive effect in the paclitaxel-induced peripheral neuropathy model and the development of recombinant human Meteorin could be a novel and effective therapeutic for chemotherapy-induced peripheral neuropathy treatment. PERSPECTIVE: Chemotherapy neuropathy is a major clinical problem that decreases quality of life for cancer patients and survivors. Our experiments demonstrate that Meteorin treatment alleviates pain-related behaviors, and signs of neurotoxicity in a mouse model of paclitaxel neuropathy.
MeSH term(s)	Humans ; Mice ; Male ; Female ; Animals ; Paclitaxel/toxicity ; Quality of Life ; Hyperalgesia/chemically induced ; Hyperalgesia/drug therapy ; Hyperalgesia/metabolism ; Neuralgia/chemically induced ; Neuralgia/drug therapy ; Antineoplastic Agents/adverse effects ; Analgesics/therapeutic use ; Antineoplastic Agents, Phytogenic/toxicity
Chemical Substances	Paclitaxel (P88XT4IS4D) ; Antineoplastic Agents ; Analgesics ; Antineoplastic Agents, Phytogenic
Language	English
Publishing date	2022-11-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2018789-0
ISSN	1528-8447 ; 1526-5900
ISSN (online)	1528-8447
ISSN	1526-5900
DOI	10.1016/j.jpain.2022.10.015
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Article: Transcriptome Analysis of the Human Tibial Nerve Identifies Sexually Dimorphic Expression of Genes Involved in Pain, Inflammation, and Neuro-Immunity.

Ray, Pradipta R / Khan, Jawad / Wangzhou, Andi / Tavares-Ferreira, Diana / Akopian, Armen N / Dussor, Gregory / Price, Theodore J

Frontiers in molecular neuroscience

2019 Volume 12, Page(s) 37

Abstract: Sex differences in gene expression are important contributors to normal physiology and mechanisms of disease. This is increasingly apparent in understanding and potentially treating chronic pain where molecular mechanisms driving sex differences in ... ...

Abstract	Sex differences in gene expression are important contributors to normal physiology and mechanisms of disease. This is increasingly apparent in understanding and potentially treating chronic pain where molecular mechanisms driving sex differences in neuronal plasticity are giving new insight into why certain chronic pain disorders preferentially affect women vs. men. Large transcriptomic resources are now available and can be used to mine for sex differences to gather insight from molecular profiles using donor cohorts. We performed in-depth analysis of 248 human tibial nerve (hTN) transcriptomes from the GTEx Consortium project to gain insight into sex-dependent gene expression in the peripheral nervous system (PNS). We discover 149 genes with sex differential gene expression. Many of the more abundant genes in men are associated with inflammation and appear to be primarily expressed by glia or immune cells, with some genes downstream of Notch signaling. In women, we find the differentially expressed transcription factor SP4 that is known to drive a regulatory program, and may impact sex differences in PNS physiology. Many of these 149 differentially expressed (DE) genes have some previous association with chronic pain but few of them have been explored thoroughly. Additionally, using clinical data in the GTEx database, we identify a subset of DE, sexually dimorphic genes in diseases associated with chronic pain: arthritis and Type II diabetes. Our work creates a unique resource that identifies sexually dimorphic gene expression in the human PNS with implications for discovery of sex-specific pain mechanisms.
Language	English
Publishing date	2019-03-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2019.00037
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