Articles: neuropathic-pain.
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Transl Perioper Pain Med · Jan 2020
Long noncoding RNA H19 in the injured dorsal root ganglion contributes to peripheral nerve injury-induced pain hypersensitivity.
Peripheral nerve injury-induced changes in gene transcription and translation in the dorsal root ganglion (DRG) play a critical role in the development and maintenance of neuropathic pain. Long noncoding RNAs (lncRNAs) regulate gene expression. Here, we report that peripheral nerve injury caused by ligation of the fourth spinal nerve (SNL) led to a time-dependent increase in the expression in H19, an lncRNA, in the injured DRG. ⋯ DRG microinjection of neither siRNA affected locomotor activity and acute basal responses to mechanical and thermal stimuli. Our findings suggest that H19 participates in the peripheral mechanism underlying the development and maintenance of neuropathic pain. H19 may be a potential target for treatment of this disorder.
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Transient receptor potential ankyrin 1 (TRPA1) is well documented as an important molecule in pain hypersensitivity following inflammation and nerve injury and in many other cellular biological processes. Here, we show that TRPA1 is expressed not only by sensory neurons of the dorsal root ganglia (DRG) but also in their adjacent satellite glial cells (SGCs), as well as nonmyelinating Schwann cells. TRPA1 immunoreactivity is also detected in various cutaneous structures of sensory neuronal terminals, including small and large caliber cutaneous sensory fibers and endings. ⋯ SGCs and neurons harvested from DRG proximal to painful tissue inflammation induced by plantar injection of complete Freund's adjuvant show greater AITC-evoked elevation of [Ca2+]i and slower recovery compared to sham controls. Similar TRPA1 sensitization occurs in both SGCs and neurons during neuropathic pain induced by spared nerve injury. Together, these results show that functional TRPA1 is expressed by sensory ganglia SGCs, and TRPA1 function in SGCs is enhanced after both peripheral inflammation and nerve injury, and suggest that TRPA1 in SGCs may contribute to inflammatory and neuropathic pain.
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Frontiers in pharmacology · Jan 2020
ReviewDrug Repositioning for the Prevention and Treatment of Chemotherapy-Induced Peripheral Neuropathy: A Mechanism- and Screening-Based Strategy.
Chemotherapy-induced peripheral neuropathy (CIPN) is a severe adverse effect observed in most patients treated with neurotoxic anti-cancer drugs. Currently, there are no therapeutic options available for the prevention of CIPN. Furthermore, few drugs are recommended for the treatment of existing neuropathies because the mechanisms of CIPN remain unclear. ⋯ Cancer chemotherapy is performed in a planned manner; therefore, preventive strategies can be planned for CIPN. Drug repositioning studies, which identify the unexpected actions of already approved drugs, have increased in recent years. We have also focused on drug repositioning studies, especially for prevention, because they should be rapidly translated to patients suffering from CIPN.