The prokineticin system and glia cells as pharmacological targets to control neuroinflammation and to relieve pain in a murine model of Fabry–Anderson disease

Neuropathic pain is a major symptom of Fabry-Anderson disease (FD). It develops in childhood, is life-lasting, and resists current therapies; finding new therapeutic strategies is urgently needed. We demonstrate that neuroinflammation control effectively relieves FD pain. We used 2 pharmacological approaches: the microglial inhibitor minocycline and the block of the activity of the chemokine prokineticin-2 with the specific receptor antagonist PC1 (patented compound 1). Ten- and 25-week-old male GLA-/- mice (the FD murine model) were used. These mice were characterized by mechanical allodynia, thermal hyperalgesia, hyposensitivity to cold stimuli, and abdominal pain. Two weeks of treatment with minocycline or PC1 successfully counteracted sensory alterations. A significant inflammatory state, characterized by high levels of prokineticin-2 and proinflammatory cytokines, was present in the FD gut. The sciatic nerve showed initial severe neuroinflammation that attenuated over time. In dorsal root ganglia, neuroinflammation was severe and persistent with prokineticin-2, proinflammatory cytokines, ionized calcium-binding adapter molecule 1, and glial fibrillary acidic protein overexpression; histone demethylases KDM6A and B were also upregulated. We highlighted neuroinflammation in the spinal cord that increased over time. Treatment with minocycline or PC1 significantly counteracted inflammation and neuroinflammation, reducing prokineticin-2 and proinflammatory cytokines levels and increasing anti-inflammatory factor PPARγ expression. Both treatments prevented the onset of micro- and astrogliosis in the spinal cord. We underline the role of neuroinflammation and microglia in FD pain and suggest that treatments that control the activity of the prokineticin system, glial activation, and the production of proinflammatory cytokines and increase anti-inflammatory mediators have a therapeutic effect on pain in FD.

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Publication Details

Journal
Pain
Published
2025-09-25
DOI
https://doi.org/10.1097/j.pain.0000000000003818
Citations
3
Primary Topic
Lysosomal Storage Disorders Research
Type
article
Field-Weighted Citation Impact
3.49
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article

The prokineticin system and glia cells as pharmacological targets to control neuroinflammation and to relieve pain in a murine model of Fabry–Anderson disease

Valentina Onnis, Sanzio Candeletti, Giada Amodeo, Benedetta Riboldi et al.
3 citations
Pain
Lysosomal Storage Disorders Research
3.49
article

The prokineticin system and glia cells as pharmacological targets to control neuroinflammation and to relieve pain in a murine model of Fabry–Anderson disease

Valentina Onnis, Sanzio Candeletti, Giada Amodeo, Benedetta Riboldi, Silvia Franchi, Loredana Maria Losapio, Laura Rullo, Stefania Ceruti, Giulia Magni, Davide Moi, Paola Sacerdote, Giulia Galimberti, Patrizia Romualdi
article en
3 citations

Abstract

Neuropathic pain is a major symptom of Fabry-Anderson disease (FD). It develops in childhood, is life-lasting, and resists current therapies; finding new therapeutic strategies is urgently needed. We demonstrate that neuroinflammation control effectively relieves FD pain. We used 2 pharmacological approaches: the microglial inhibitor minocycline and the block of the activity of the chemokine prokineticin-2 with the specific receptor antagonist PC1 (patented compound 1). Ten- and 25-week-old male GLA-/- mice (the FD murine model) were used. These mice were characterized by mechanical allodynia, thermal hyperalgesia, hyposensitivity to cold stimuli, and abdominal pain. Two weeks of treatment with minocycline or PC1 successfully counteracted sensory alterations. A significant inflammatory state, characterized by high levels of prokineticin-2 and proinflammatory cytokines, was present in the FD gut. The sciatic nerve showed initial severe neuroinflammation that attenuated over time. In dorsal root ganglia, neuroinflammation was severe and persistent with prokineticin-2, proinflammatory cytokines, ionized calcium-binding adapter molecule 1, and glial fibrillary acidic protein overexpression; histone demethylases KDM6A and B were also upregulated. We highlighted neuroinflammation in the spinal cord that increased over time. Treatment with minocycline or PC1 significantly counteracted inflammation and neuroinflammation, reducing prokineticin-2 and proinflammatory cytokines levels and increasing anti-inflammatory factor PPARγ expression. Both treatments prevented the onset of micro- and astrogliosis in the spinal cord. We underline the role of neuroinflammation and microglia in FD pain and suggest that treatments that control the activity of the prokineticin system, glial activation, and the production of proinflammatory cytokines and increase anti-inflammatory mediators have a therapeutic effect on pain in FD.

PainVol. 167(2)
University of Cagliari (IT), University of Milan (IT), University of Bologna (IT)
Openalex Percentile: Top 7%
Lysosomal Storage Disorders Research
3.49
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