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DGCR5 attenuates neuropathic pain through sponging miR‐330‐3p and regulating PDCD4 in CCI rat models
Author(s) -
Peng Chengwei,
Zhang Chuanqing,
Su Zhe,
Lin Dongyang
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27487
Subject(s) - neuropathic pain , medicine , downregulation and upregulation , hyperalgesia , nociception , neuroinflammation , sciatic nerve , inflammation , neuroscience , pharmacology , biology , receptor , gene , biochemistry
Neuropathic pain caused by somatosensory nervous system dysfunction is a serious public health problem. Some long noncoding RNAs (lncRNAs) can participate in physiological processes involved in neuropathic pain. However, the effects of lncRNA DGCR5 in neuropathic pain have not been explored. Therefore, in our current study, we concentrated on the biological roles of DGCR5 in neuropathic pain. Here, it was observed that DGCR5 was significantly decreased in chronic sciatic nerve injury (CCI) rat models. DGCR5 overexpression was able to alleviate neuropathic pain development including mechanical and thermal hyperalgesia. In addition, the current understanding of miR‐330‐3p function in neuropathic pain remains largely incomplete. Here, we found that miR‐330‐3p was greatly increased in CCI rats and DGCR5 can modulate miR‐330‐3p expression negatively. Upregulation of DGCR5 repressed inflammation‐correlated biomarkers including interleukin 6 (IL‐6), tumor necrosis factor α, and IL‐1β in CCI rats by sponging miR‐330‐3p. The negative correlation between DGCR5 and miR‐330‐3p was confirmed in our current study. Inhibition of miR‐330‐3p suppressed neuropathic pain progression by restraining neuroinflammation in vivo. In addition, PDCD4 was predicted as a downstream target of miR‐330‐3p. Furthermore, PDCD4 was significantly increased in CCI rats and DGCR5 regulated PDCD4 expression through sponging miR‐330‐3p in CCI rat models. Taken these together, it was implied that DGCR5/miR‐330‐3p/PDCD4 axis participated in neuropathic pain treatment.