Papel del microRNA-30c en la percepción dolorosa

Abstract

I appreciate that miR-30c is responsible for the development of allodynia after traumatic neuropathy but not after ischemic neuropathy. Acute treatment with miR-30c or anti-miR-30c don't change nociceptive evoked responses in acute pain models thermal, mechanical and chemical type. Only anti-miR-30c reduced central sensitization responses by chemical stimulus. Chronic treatment with miR-30c accelerated and enhanced mechanical allodynia after traumatic injury and anti-miR-30c attenuated and delayed allodynia. . Medullary levels of messenger RNA expression target of miR-30c, TGF-ß1 and SMAD-1, were inversely correlated with miR-30c. Furthermore, treatment with miR-30c inhibitor significantly increased the expression of both core messenger RNAs. We can apply the value of miR-30c as a potential therapeutic target for the treatment of neuropathic pain of traumatic origin, and suggest their usefulness as a prognostic biomarker diagnosis and / or treatment response.