Li‐Jun Zhi
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Li‐Jun Zhi has a total of 4 co-authors. Here are the top co-authors by number of shared publications:
- Fang Wang
Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
1 shared publication - Juan Liu
Operating Room, Huai'an Second People's Hospital, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, China
1 shared publication Liang Zhong
Department of Anesthesiology, Wuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College Huazhong University of Science & Technology Wuhan China
1 shared publicationWeimin Xiao
The Department of Anesthesiology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan China
1 shared publication
Latest Publications
- 3 June 2019
- Published by Wiley in Journal of Cellular Biochemistry
- Vol. 120 (10) , 16614-16623
miR‐21‐5p inhibits neuropathic pain development via directly targeting C‐C motif ligand 1 and tissue inhibitor of metalloproteinase‐3
MicroRNAs (miRNA) play important roles in neuroinflammation and neuropathic pain development; however, the underlying mechanism requires further investigation. The expression of miR‐21‐5p was remarkably upregulated in chronic constrictive injury (CCI) rat model. A significant alleviated neuropathic pain development and reduced the expression of cytokines was observed in CCI rat after exogenous injection of miR‐21‐5p mimic. The dual‐luciferase analysis revealed that tissue inhibitor of metalloproteinase‐3 (TIMP3) and chemokines C‐C motif ligand 1 (CCL1) was direct downstream target of miR‐21‐5p. Moreover, silencing of TIMP3 and CCL1 could rescue mechanical allodynia, thermal hyperalgesia and cytokine release in CCI rat, suggesting that TIMP3 and CCL1 exert their function by mediating neuroinflammation in neuropathic pain development. Therefore, we have identified a novel miR‐21‐5p–CCL1/TIMP3‐cytokine axis in regulation of neuropathic pain development in CCI rat model, which is valuable for enhancing our understanding of neuropathic pain and developing miRNAs as potential therapeutic options in the future.
- 3 June 2019
- Published by Wiley in Journal of Cellular Biochemistry
- Vol. 120 (10) , 16614-16623
miR‐21‐5p inhibits neuropathic pain development via directly targeting C‐C motif ligand 1 and tissue inhibitor of metalloproteinase‐3
MicroRNAs (miRNA) play important roles in neuroinflammation and neuropathic pain development; however, the underlying mechanism requires further investigation. The expression of miR‐21‐5p was remarkably upregulated in chronic constrictive injury (CCI) rat model. A significant alleviated neuropathic pain development and reduced the expression of cytokines was observed in CCI rat after exogenous injection of miR‐21‐5p mimic. The dual‐luciferase analysis revealed that tissue inhibitor of metalloproteinase‐3 (TIMP3) and chemokines C‐C motif ligand 1 (CCL1) was direct downstream target of miR‐21‐5p. Moreover, silencing of TIMP3 and CCL1 could rescue mechanical allodynia, thermal hyperalgesia and cytokine release in CCI rat, suggesting that TIMP3 and CCL1 exert their function by mediating neuroinflammation in neuropathic pain development. Therefore, we have identified a novel miR‐21‐5p–CCL1/TIMP3‐cytokine axis in regulation of neuropathic pain development in CCI rat model, which is valuable for enhancing our understanding of neuropathic pain and developing miRNAs as potential therapeutic options in the future.