ArticleMolecular pain2016
Crosstalk between astrocytic CXCL12 and microglial CXCR4 contributes to the development of neuropathic pain.
Article in Molecular pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- Molecular insights into glial neuroimmune cross reactivity with CNS antigens and its role in neuroinflammation.Inflammopharmacology · 2026Pooled it
- Neuroplasticity-Driven Mechanisms and Therapeutic Targets in the Anterior Cingulate Cortex in Neuropathic Pain.Brain and behavior · 2026Review
- Decoding Neuroinflammatory Pathways: The Role of the CXCL12-CXCR4/CXCR7 Axis in ALS-Related Cognitive Impairment.Molecular neurobiology · 2026Review
- Associations between serum inflammatory mediators and chronic pain after laparoscopic inguinal hernia repair in elderly patients.Frontiers in human neuroscience · 2026Article
- Early pharmacological blockade of the CXCL12-CXCR4 axis attenuates vertebral hypercalcification in a zebrafish model of pseudoxanthoma elasticum.Biochemistry and biophysics reports · 2025Article
- Exploring the Role of RhoA/ROCK Signaling in Pain: A Narrative Review.Aging and disease · 2025Review
- The role of CXCL12/CXCR4/CXCR7 axis in cognitive impairment associated with neurodegenerative diseases.Brain, behavior, & immunity - health · 2025Review
- Exploring potential mechanistic aspects of "Biaoben acupoint" acupuncture for lumbar disc herniation using 4D proteomics.Frontiers in neurology · 2025Article
- Elevated plasma CXCL12 leads to pain chronicity via positive feedback upregulation of CXCL12/CXCR4 axis in pain synapses.The journal of headache and pain · 2024Article
- Inhibiting the JNK Signaling Pathway Attenuates Hypersensitivity and Anxiety-Like Behavior in a Rat Model of Non-specific Chronic Low Back Pain.Journal of molecular neuroscience : MN · 2024Article
- Blocking IL-17A prevents oxycodone-induced depression-like effects and elevation of IL-6 levels in the ventral tegmental area and reduces oxycodone-derived physical dependence in rats.Brain, behavior, and immunity · 2024Article
- Spinal Cord Injury Affects Gene Expression of Transmembrane Proteins in Tissue and Release of Extracellular Vesicle in Blood: In Silico andCell journal · 2023Article
- CD13 facilitates immune cell migration and aggravates acute injury but promotes chronic post-stroke recovery.Journal of neuroinflammation · 2023Article
- Targeting Members of the Chemokine Family as a Novel Approach to Treating Neuropathic Pain.Molecules (Basel, Switzerland) · 2023Review
- Article
- CXCL13 contributes to chronic pain of a mouse model of CRPS-I via CXCR5-mediated NF-κB activation and pro-inflammatory cytokine production in spinal cord dorsal horn.Journal of neuroinflammation · 2023Article
- Neuropathic pain; what we know and what we should do about it.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- The Role of Neuroinflammation in Complex Regional Pain Syndrome: A Comprehensive Review.Journal of pain research · 2023Review
- Astrocyte-microglia interaction through C3/C3aR pathway modulates neuropathic pain in rats model of chronic constriction injury.Molecular pain · 2022Article
- Lidocaine ameliorates chronic constriction injury-induced neuropathic pain through regulating M1/M2 microglia polarization.Open medicine (Warsaw, Poland) · 2022Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChemokine axis chemokine C-X-C motif ligand 12/C-X-C chemokine receptor type 4 (CXCL12/CXCR4) is an emerging pain modulator, but mechanisms for its involvement in neuropathic pain remain unclear. Here, we aimed to study whether CXCL12/CXCR4 axis modulated the development of neuropathic pain via glial mechanisms. In this study, two mouse models of neuropathic pain, namely partial sciatic nerve ligation (pSNL) model and chronic post-ischemia pain (CPIP) model, were used.
resultsIn the dorsal horn of L3-L5 segment of spinal cord, CXCL12 and CXCR4 were expressed in both astrocyte and microglia in normal mice. In the pSNL or CPIP model, the expression level of CXCL12 in the ipsilateral L3-L5 segment of mice spinal cord was increased in an astrocyte-dependent manner on post-operative day (POD) 3. Intrathecal administration of CXCL12 with AMD3100 (CXCR4 antagonist) or minocycline (microglia activation inhibitor), but not fluorocitrate (astrocyte activation inhibitor), reversed CXCL12-indued mechanical allodynia in naïve mice. In these models, AMD3100 and AMD3465 (CXCR4 antagonist), administered daily from 1 h before surgery and up to POD 3, attenuated the development of mechanical allodynia. Moreover, AMD3100 administered daily from 1 h before surgery and up to POD 3 downregulated mRNA levels of tumor necrosis factor alpha, interleukin 1β, and interleukin 6 in the ipsilateral L3-L5 segment of spinal cord in the pSNL and CPIP models on POD 3.
conclusionThis study demonstrates the crosstalk between astrocytic CXCL12 and microglial CXCR4 in the pathogenesis of neuropathic pain using pSNL and CPIP models. Our results offer insights for the future research on CXCL12/CXCR4 axis and neuropathic pain therapy.
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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.