Chronic Low Back Pain (CLBP) is an inflammatory condition that may originate from an injury, disease or stress on tendons, ligaments and discus of the spinal structure. It is known that neuroinflammatory processes are pathologichallmarks of CLBP that lead to the release of proinflammatory molecules that increase nociceptors sensitization, pain hypersensitivity or hyperalgesia. Transient Receptor Potential (TRP) channels are known to act as receptors of various stimuli in peripheral sensory neurons and in other somatic structure. Numerous studies highlighted the activation and/or sensitization of these channels during inflammation as the major mechanism underlying neuropathic and inflammatory pain. In order to investigate the roleplayed and to classify TRPs channels in samples from 6 patients affected by CLBP, the TRPs expression was measured and morphological, ultrastructural and immunohistochemical alterations were analyzed. Immunofluorescence and expression analyses showed a significant increase in the levels of TRPs (A1, V1, V2, V4 and M8) in the pathological capsule compared to control tissues. Interesting, in each patient analyzed, we found an over-expression of TRPV4, independently by the location and number of affected sites. Moreover, using silver impregnation, it was shown that in CLBP patients the capsular connective tissue appeared degraded and infiltrated by sensitive unmyelinated nervous fibers. The findings confirm the involvement of TRP channels, in particularly of the TRPV4 and TRPM8 in CLBP pathological condition suggesting that these channels could represent a target for new therapeutic approaches.
TRP channels expression in Chronic Low Back Pain
FOZZATO, STEFANIA;Baranzini N;Bossi E;ROSETI, CRISTINA
;Cinquetti R;Grimaldi ANNALISA;Campomenosi p;Surace MF
2019-01-01
Abstract
Chronic Low Back Pain (CLBP) is an inflammatory condition that may originate from an injury, disease or stress on tendons, ligaments and discus of the spinal structure. It is known that neuroinflammatory processes are pathologichallmarks of CLBP that lead to the release of proinflammatory molecules that increase nociceptors sensitization, pain hypersensitivity or hyperalgesia. Transient Receptor Potential (TRP) channels are known to act as receptors of various stimuli in peripheral sensory neurons and in other somatic structure. Numerous studies highlighted the activation and/or sensitization of these channels during inflammation as the major mechanism underlying neuropathic and inflammatory pain. In order to investigate the roleplayed and to classify TRPs channels in samples from 6 patients affected by CLBP, the TRPs expression was measured and morphological, ultrastructural and immunohistochemical alterations were analyzed. Immunofluorescence and expression analyses showed a significant increase in the levels of TRPs (A1, V1, V2, V4 and M8) in the pathological capsule compared to control tissues. Interesting, in each patient analyzed, we found an over-expression of TRPV4, independently by the location and number of affected sites. Moreover, using silver impregnation, it was shown that in CLBP patients the capsular connective tissue appeared degraded and infiltrated by sensitive unmyelinated nervous fibers. The findings confirm the involvement of TRP channels, in particularly of the TRPV4 and TRPM8 in CLBP pathological condition suggesting that these channels could represent a target for new therapeutic approaches.
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