ArticleThe European journal of neuroscience2010
Alterations of CXCR4 function in μ-opioid receptor-deficient glia.
Article in The European journal of neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- LPA1-mediated inhibition of CXCR4 attenuates CXCL12-induced signaling and cell migration.Cell communication and signaling : CCS · 2023Article
- Cellular, synaptic, and network effects of chemokines in the central nervous system and their implications to behavior.Pharmacological reports : PR · 2021Review
- Opioid and chemokine regulation of cortical synaptodendritic damage in HIV-associated neurocognitive disorders.Brain research · 2019Review
- Novel Positive Allosteric Modulators of Glutamate Transport Have Neuroprotective Properties in an in Vitro Excitotoxic Model.ACS chemical neuroscience · 2019Article
- In vivo opioid receptor heteromerization: where do we stand?British journal of pharmacology · 2015Review
- Interactive HIV-1 Tat and morphine-induced synaptodendritic injury is triggered through focal disruptions in Na⁺ influx, mitochondrial instability, and Ca²⁺ overload.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Neuronal ferritin heavy chain and drug abuse affect HIV-associated cognitive dysfunction.The Journal of clinical investigation · 2014Article
- Functions of the chemokine receptor CXCR4 in the central nervous system and its regulation by μ-opioid receptors.International review of neurobiology · 2014Review
- CXCL12 signaling in the development of the nervous system.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012Review
- Opiate drug use and the pathophysiology of neuroAIDS.Current HIV research · 2012Review
- Differential expression and HIV-1 regulation of μ-opioid receptor splice variants across human central nervous system cell types.Journal of neurovirology · 2012Article
- Toll-like receptors in chronic pain.Experimental neurology · 2012Review
- Regulation of neuronal ferritin heavy chain, a new player in opiate-induced chemokine dysfunction.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Review
- Morphine potentiates neurodegenerative effects of HIV-1 Tat through actions at μ-opioid receptor-expressing glia.Brain : a journal of neurology · 2011Article
- Exploring the neuroimmunopharmacology of opioids: an integrative review of mechanisms of central immune signaling and their implications for opioid analgesia.Pharmacological reviews · 2011Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The chemokine receptor CXCR4 and the μ-opioid receptor (MOR) are G-protein-coupled receptors that are essential for normal function of the nervous and immune systems. Several studies have suggested that MOR is a key regulator of CXCR4 in the brain; however, the molecular basis of the opioid-chemokine interaction is not fully understood, and it may involve different mechanisms in neuronal and glial cells. Our previous studies demonstrated that MOR stimulation specifically upregulates the protein ferritin heavy chain - an inhibitor of CXCR4 - in neurons, and suggested that additional mechanisms could be operative in glia. In this study, we investigated CXCR4 function in brains and astroglial cultures deprived of MOR. Reduced coupling of CXCR4 to G-proteins was found in brain slices and tissue homogenates of MOR(-/-) mice as compared with wild-type controls. CXCR4-induced signaling was also reduced in glial cultures from MOR(-/-) mice, as shown by analysis of CXCR4 downstream targets (Akt and ERK1/2). Pharmacological studies with δ-opioid receptor (DOR)-specific ligands suggested that DOR-CXCR4 interactions are implicated in the inhibition of CXCR4 in MOR-deficient cells both in vitro and in vivo. Moreover, increased CXCR4/DOR co-immunoprecipitation was found in brain tissue and cultured glia from MOR(-/-) mice. Importantly, CXCR4 function was restored by pretreatment with a DOR antagonist. Overall, these findings indicate that DOR plays a crucial role in the regulation of CXCR4 in glia, probably via silent receptor heterodimers. The data also suggest that the opiate system interferes with normal CXCR4 function in different ways, depending on receptor subtypes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.