Imperial College London

ProfessorPraveenAnand

Faculty of MedicineDepartment of Brain Sciences

Professor
 
 
 
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Contact

 

+44 (0)20 3313 3319p.anand

 
 
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Location

 

Area A Grd FloorUnknownHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Donatien:2018:10.1097/PR9.0000000000000676,
author = {Donatien, P and Anand, U and Yiangou, Y and Sinisi, M and Fox, M and MacQuillan, A and Quick, T and Korchev, YE and Anand, P},
doi = {10.1097/PR9.0000000000000676},
journal = {PAIN Reports},
pages = {e676--e676},
title = {Granulocyte-macrophage colony-stimulating factor receptor expression in clinical pain disorder tissues and role in neuronal sensitization},
url = {http://dx.doi.org/10.1097/PR9.0000000000000676},
volume = {3},
year = {2018}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Introduction: Granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR) is highly expressed in peripheral macrophages and microglia, and is involved in arthritis and cancer pain in animal models. However, there is limited information on GM-CSFR expression in human central nervous system (CNS), peripheral nerves, or dorsal root ganglia (DRG), particularly in chronic pain conditions. Objectives: Immunohistochemistry was used to quantify GM-CSFR expression levels in human tissues, and functional sensory effects of GM-CSF were studied in cultured DRG neurons. Results: Granulocyte-macrophage colony-stimulating factor receptor was markedly increased in microglia at lesional sites of multiple sclerosis spinal cords (P = 0.01), which co-localised with macrophage marker CD68 (P = 0.009). In human DRG, GM-CSFR was expressed in a subset of small/medium diameter cells (30%) and few large cells (10%), with no significant change in avulsion-injured DRG. In peripheral nerves, there was a marked decrease in axonal GM-CSFR after chronic painful nerve injury (P = 0.004) and in painful neuromas (P = 0.0043); CD-68-positive macrophages were increased (P = 0.017) but did not appear to express GM-CSFR. Although control synovium showed absent GM-CSFR immunostaining, this was markedly increased in macrophages of painful osteoarthritis knee synovium. Granulocyte-macrophage colony-stimulating factor receptor was expressed in 17 ± 1.7% of small-/medium-sized cultured adult rat DRG neurons, and in 27 ± 3.3% of TRPV1-positive neurons. Granulocyte-macrophage colony-stimulating factor treatment sensitized capsaicin responses in vitro, which were diminished by p38 MAPK or TrkA inhibitors. Conclusion: Our findings support GM-CSFR as a therapeutic target for pain and hypersensitivity in clinical CNS and peripheral inflammatory conditions. Although GM-CSFR was decreased in chronic painful injured peripheral nerves, it could mediate CNS neuroinflammatory effects, which deserves
AU - Donatien,P
AU - Anand,U
AU - Yiangou,Y
AU - Sinisi,M
AU - Fox,M
AU - MacQuillan,A
AU - Quick,T
AU - Korchev,YE
AU - Anand,P
DO - 10.1097/PR9.0000000000000676
EP - 676
PY - 2018///
SN - 2471-2531
SP - 676
TI - Granulocyte-macrophage colony-stimulating factor receptor expression in clinical pain disorder tissues and role in neuronal sensitization
T2 - PAIN Reports
UR - http://dx.doi.org/10.1097/PR9.0000000000000676
UR - https://www.ncbi.nlm.nih.gov/pubmed/30534627
UR - http://hdl.handle.net/10044/1/91660
VL - 3
ER -