Interleukin 6 decreases nociceptor expression of the potassium channel KV1.4 in a rat model of hand-arm vibration syndrome
| Autor: | Pedro Alvarez, Oliver Bogen, Jon D. Levine |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Male
Hindlimb Medical and Health Sciences Rats Sprague-Dawley 0302 clinical medicine 030202 anesthesiology Anesthesiology Musculoskeletal Pain Ganglia Spinal 2.1 Biological and endogenous factors Aetiology Hand-Arm Vibration Syndrome Gene knockdown biology Chemistry Pain Research Skeletal Potassium channel Neurology Hyperalgesia Gene Knockdown Techniques Nociceptor Muscle Kv1.4 Potassium Channel Chronic Pain medicine.medical_specialty Spinal Chronic musculoskeletal pain Vibration Article 03 medical and health sciences Gastrocnemius muscle Downregulation and upregulation Internal medicine medicine Nociceptor hyperexcitability Animals Interleukin 6 Muscle Skeletal Cytokine Inflammation Animal Interleukin-6 Psychology and Cognitive Sciences Neurosciences Glycoprotein 130 Rats Disease Models Animal Anesthesiology and Pain Medicine Endocrinology Musculoskeletal Disease Models biology.protein Ganglia Neurology (clinical) Sprague-Dawley 030217 neurology & neurosurgery |
| Zdroj: | Pain Pain, vol 160, iss 8 |
| ISSN: | 1872-6623 |
| Popis: | Chronic muscle pain is a prominent symptom of the hand-arm vibration syndrome (HAVS), an occupational disease induced by exposure to vibrating power tools, but the underlying mechanism remains unknown. We evaluated the hypothesis that vibration induces an interleukin 6 (IL-6)-mediated downregulation of the potassium voltage-gated channel subfamily A member 4 (KV1.4) in nociceptors leading to muscle pain. Adult male rats were submitted to a protocol of mechanical vibration of the right hind limb. Twenty-four hours after vibration, muscle hyperalgesia was observed, concomitant to increased levels of IL-6 in the gastrocnemius muscle and decreased expression of KV1.4 in the dorsal root ganglia. Local injection of neutralizing antibodies against IL-6 attenuated the muscle hyperalgesia induced by vibration, whereas antisense knockdown of this channel in the dorsal root ganglia mimicked the muscle hyperalgesia observed in the model of HAVS. Finally, knockdown of the IL-6 receptor signaling subunit glycoprotein 130 (gp130) attenuated both vibration-induced muscle hyperalgesia and downregulation of KV1.4. These results support the hypothesis that IL-6 plays a central role in the induction of muscle pain in HAVS. This likely occurs through intracellular signaling downstream to the IL-6 receptor subunit gp130, which decreases the expression of KV1.4 in nociceptors. |
| Databáze: | OpenAIRE |
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