Fractalkine/CX3CL1 and its receptor CX3CR1 in the anterior cingulate cortex of the experimental model of neuropathic pain
| Autoři | |
|---|---|
| Rok publikování | 2021 |
| Druh | Konferenční abstrakty |
| Fakulta / Pracoviště MU | |
| Citace | |
| Popis | 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 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 (n=8) were immunostained for cellular detection of CX3CL1/CX3CR1, CathepsinS, and ADAM17 under the same conditions. Immunofluorescence (IF) intensity was measured using our standard protocol. Moreover, CX3CL1, CX3CR1, and CathepsinS protein levels were assessed using western blot analysis. We found that SCI induced increased IF for both CX3CL1 and CX3CR1 in the ACC neurons of the lamina 2/3 when compared with controls. The increased protein levels were verified by western blot analysis. CathepsinS-IF and ADAM17-IF were also observed in the ACC neurons while western blot failed to detect CathepsinS protein levels. The biological activity of CX3CL1 is regulated by the conversion of a membrane integrated into a soluble form. Our results of immunofluorescence staining suggested that neuronal sCX3CL1 in ACC after SCI may act in an autocrine manner to be involved in neuroprotection. Supported by MUNI/A/1520/2020 and La MARATÓ de TV3 Foundation (201705.30.31). |
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