Neuronal upregulation of chemokines and their receptors in the anterior cingulate cortex of the experimental model of neuropathic pain
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| Year of publication | 2021 |
| Type | Conference abstract |
| MU Faculty or unit | |
| Citation | |
| Description | The anterior cingulate cortex (ACC) mediates the affective component of neuropathic pain responses. Given the strategic functions of chemokines in chemoattraction, the study of the functional involvement of CX3CL1/CX3CR1 and CCL2/CCR2 signaling in the brain was focused on neuron-microglia interactions, neglecting the signaling role in neurons by an autocrine manner. Female adult CD1 Swiss mice were operated on the spinal nerve injury (SCI) by contusion using weight drop apparatus following dorsal laminectomy at T8-T9 (n=16). Naive and sham-operated mice were used as controls. Operated animals were left to survive for 6 or 12 weeks. Coronal cryostat sections through ACC were immunostained for cellular detection of CX3CL1/CX3CR1, CCL2/CCR2 CathepsinS, and ADAM17 under the same conditions. Immunofluorescence (IF) intensity was measured using our standard protocol. Moreover, protein levels of chemokines, their receptors, CathepsinS and ADAM17 were assessed using western blot analysis. We found that SCI induced increased IF for both CX3CL1/CX3CR1 and CCL2/CCR2 chemokine axis in the ACC neurons of the lamina 2/3 when compared with controls. The increased protein levels were verified by western blot analysis. CathepsinS- and ADAM17-IF were also observed in the ACC neurons. This indicated that the biological activity of neuronal CX3CL1 is regulated by the conversion of membrane-integrated to soluble form. In summary, our results of neuronal immunostaining of both CX3CL1 and CCL2 as well as their receptors in ACC suggested that CX3CL1/CX3CR1 and CCL2/CCR2 chemokine axis may act in an autocrine manner to be involved in neuromodulation or neuroprotection after SCI. Supported by La MARATÓ de TV3 Foundation (201705.30.31) and MUNI/A/1520/2020. |
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