Cyclooxygenase-2 (Cox-2) in injured human nerve and a rat model of nerve injury.
Inflammation associated with nerve injury produces a number of pathogenic chemical mediators of which prostanoids are a potent component. Cyclooxygenases (Cox-1 and Cox-2) are the enzymes responsible for prostanoid production. We have investigated Cox-2 immunoreactivity (Cox-2-IR) and glial activati...
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| Fformat: | Journal article |
| Iaith: | English |
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2004
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| _version_ | 1826304636603072512 |
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| author | Durrenberger, P Facer, P Gray, R Chessell, I Naylor, A Bountra, C Banati, R Birch, R Anand, P |
| author_facet | Durrenberger, P Facer, P Gray, R Chessell, I Naylor, A Bountra, C Banati, R Birch, R Anand, P |
| author_sort | Durrenberger, P |
| collection | OXFORD |
| description | Inflammation associated with nerve injury produces a number of pathogenic chemical mediators of which prostanoids are a potent component. Cyclooxygenases (Cox-1 and Cox-2) are the enzymes responsible for prostanoid production. We have investigated Cox-2 immunoreactivity (Cox-2-IR) and glial activation in human injured (n = 16) and uninjured (n = 8) nerves and in the chronic constriction injury (CCI) model of nerve injury in the rat, using immunohistological and autoradiographic methods. Tissues were immunostained with antibodies to Cox-2, CD-68 (human macrophage marker), OX42 (rat microglial marker), or incubated with tritiated PK11195 (marker of glial activation), prior to image analysis. In human nerves, Cox-2-IR was detected in cells with morphology and distribution similar to macrophages/microglia - these were increased significantly in human nerve proximal to injury (p < 0.002), reaching a peak at 4-6 weeks after injury. In the rat CCI model, at 40 days after injury, microglia-like cells with Cox-2-IR were increased significantly in the injured nerve (p < 0.004) and ipsilateral dorsal spinal cord (p < 0.008). PK11195-binding results were similar for Cox-2-IR in chronic injured human nerve and rat tissues. These findings suggest that Cox-2-immunoreactive cells could play a role in processes associated with Wallerian degeneration, nerve regeneration, and the development of persistent pain. Selection of patients 4-6 weeks after nerve injury would be more likely to show any efficacy of Cox-2 inhibitors. |
| first_indexed | 2024-03-07T06:20:49Z |
| format | Journal article |
| id | oxford-uuid:f2a6b10e-b529-455b-9a30-61e7146c7ca2 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T06:20:49Z |
| publishDate | 2004 |
| record_format | dspace |
| spelling | oxford-uuid:f2a6b10e-b529-455b-9a30-61e7146c7ca22022-03-27T12:05:35ZCyclooxygenase-2 (Cox-2) in injured human nerve and a rat model of nerve injury.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:f2a6b10e-b529-455b-9a30-61e7146c7ca2EnglishSymplectic Elements at Oxford2004Durrenberger, PFacer, PGray, RChessell, INaylor, ABountra, CBanati, RBirch, RAnand, PInflammation associated with nerve injury produces a number of pathogenic chemical mediators of which prostanoids are a potent component. Cyclooxygenases (Cox-1 and Cox-2) are the enzymes responsible for prostanoid production. We have investigated Cox-2 immunoreactivity (Cox-2-IR) and glial activation in human injured (n = 16) and uninjured (n = 8) nerves and in the chronic constriction injury (CCI) model of nerve injury in the rat, using immunohistological and autoradiographic methods. Tissues were immunostained with antibodies to Cox-2, CD-68 (human macrophage marker), OX42 (rat microglial marker), or incubated with tritiated PK11195 (marker of glial activation), prior to image analysis. In human nerves, Cox-2-IR was detected in cells with morphology and distribution similar to macrophages/microglia - these were increased significantly in human nerve proximal to injury (p < 0.002), reaching a peak at 4-6 weeks after injury. In the rat CCI model, at 40 days after injury, microglia-like cells with Cox-2-IR were increased significantly in the injured nerve (p < 0.004) and ipsilateral dorsal spinal cord (p < 0.008). PK11195-binding results were similar for Cox-2-IR in chronic injured human nerve and rat tissues. These findings suggest that Cox-2-immunoreactive cells could play a role in processes associated with Wallerian degeneration, nerve regeneration, and the development of persistent pain. Selection of patients 4-6 weeks after nerve injury would be more likely to show any efficacy of Cox-2 inhibitors. |
| spellingShingle | Durrenberger, P Facer, P Gray, R Chessell, I Naylor, A Bountra, C Banati, R Birch, R Anand, P Cyclooxygenase-2 (Cox-2) in injured human nerve and a rat model of nerve injury. |
| title | Cyclooxygenase-2 (Cox-2) in injured human nerve and a rat model of nerve injury. |
| title_full | Cyclooxygenase-2 (Cox-2) in injured human nerve and a rat model of nerve injury. |
| title_fullStr | Cyclooxygenase-2 (Cox-2) in injured human nerve and a rat model of nerve injury. |
| title_full_unstemmed | Cyclooxygenase-2 (Cox-2) in injured human nerve and a rat model of nerve injury. |
| title_short | Cyclooxygenase-2 (Cox-2) in injured human nerve and a rat model of nerve injury. |
| title_sort | cyclooxygenase 2 cox 2 in injured human nerve and a rat model of nerve injury |
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