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261 results on '"Xin, Wen-Jun"'

12. Ac4C Enhances the Translation Efficiency of Vegfa mRNA and Mediates Central Sensitization in Spinal Dorsal Horn in Neuropathic Pain.

Author

Xu, Ting, Wang, Jing, Wu, Yan, Wu, Jia‐Yan, Lu, Wei‐Cheng, Liu, Meng, Zhang, Su‐Bo, Xie, Dan, Xin, Wen‐Jun, and Xie, Jing‐Dun

Subjects
NEURALGIA, RNA modification & restriction, MESSENGER RNA, GENE expression, NERVOUS system injuries, TRANSVERSUS abdominis muscle
Abstract

N4‐Acetylcytidine (ac4C), a highly conserved post‐transcriptional machinery with extensive existence for RNA modification, plays versatile roles in various cellular processes and functions. However, the molecular mechanism by which ac4C modification mediates neuropathic pain remains elusive. Here, it is found that the enhanced ac4C modification promotes the recruitment of polysome in Vegfa mRNA and strengthens the translation efficiency following SNI. Nerve injury increases the expression of NAT10 and the interaction between NAT10 and Vegfa mRNA in the dorsal horn neurons, and the gain and loss of NAT10 function further confirm that NAT10 is involved in the ac4C modification in Vegfa mRNA and pain behavior. Moreover, the ac4C‐mediated VEGFA upregulation contributes to the central sensitivity and neuropathic pain induced by SNI or AAV‐hSyn‐NAT10. Finally, SNI promotes the binding of HNRNPK in Vegfa mRNA and subsequently recruits the NAT10. The enhanced interaction between HNRNPK and NAT10 contributes to the ac4C modification of Vegfa mRNA and neuropathic pain. These findings suggest that the enhanced interaction between HNRNPK and Vegfa mRNA upregulates the ac4C level by recruiting NAT10 and contributes to the central sensitivity and neuropathic pain following SNI. Blocking this cascade may be a novel therapeutic approach in patients with neuropathic pain. [ABSTRACT FROM AUTHOR]

Published
2023
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14. Supplemental Material - NFATc2-dependent epigenetic downregulation of the TSC2/Beclin-1 pathway is involved in neuropathic pain induced by oxaliplatin

Author

Liu, Meng, Mai, Jing-Wen, Luo, De-Xing, Liu, Guan-Xi, Xu, Ting, Xin, Wen-Jun, Lin, Su-Yan, and Li, Zhen-Yu

Subjects
FOS: Clinical medicine, 111702 Aged Health Care, FOS: Health sciences, 111599 Pharmacology and Pharmaceutical Sciences not elsewhere classified, 110904 Neurology and Neuromuscular Diseases, Neuroscience
Abstract

Supplemental Material for NFATc2-dependent epigenetic downregulation of the TSC2/Beclin-1 pathway is involved in neuropathic pain induced by oxaliplatin by Meng Liu, Jing-Wen Ma, De-Xing Luo, Guan-Xi Liu, Ting Xu, Wen-Jun Xin, Su-Yan Lin, and Zhen-Yu Li in Molecular Pain

Published
2023
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24. The possible involvement of JNK activation in the spinal dorsal horn in bortezomib-induced allodynia: the role of TNF-α and IL-1β

Author

Li, Zhen-Yu, Zhang, Yuan-Pei, Zhang, Su-Bo, Li, Dai, Huang, Zhen-Zhen, and Xin, Wen-Jun

Subjects
Phosphotransferases -- Analysis -- Research, Chemotherapy -- Analysis -- Research -- Health aspects, Tumor necrosis factor -- Research, Cancer -- Chemotherapy, Interleukins -- Research -- Physiological aspects, Health
Abstract

Purpose Bortezomib (BTZ), a widely used chemotherapeutic drug, is closely associated with the development of painful peripheral neuropathy, but the mechanism underlying the induction of this disorder by BTZ remains largely unclear. To examine this association, we have evaluated the activation of mitogen-activated protein kinase (MAPK) family members in the spinal dorsal horn and the role of tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) in BTZ-induced allodynia in rats. Methods Male Sprague-Dawley rats were used as the model animals. The paw withdrawal test, in which mechanical stimuli (von Frey hairs) is applied to the plantar surface of the hindpaw, was used to determine any changes in the paw withdrawal threshold of the treated rats. A PE-10 catheter was placed intrathecally to deliver TNF-α neutralizing antibody, IL-1 receptor antagonist (IL-1ra) or the c-Jun N-terminal kinase (JNK) inhibitor SP600125. The mRNA levels of various cytokines were measured by real-time quantitative PCR. The expression of TNF-α, IL-1β and mitogen-activated protein kinase (MAPK) family members in the spinal dorsal horn was measured by western blot analysis and immunohistochemistry. All data were expressed as the mean ± standard error of the mean and analyzed using the SPSS version 13.0 software program. Results The BTZ treatment induced an upsurge in the mRNA and protein levels of TNF-α in the neurons and IL-1β in the astrocytes in the spinal dorsal horn. It also significantly upregulated the phosphorylation of JNK but not of extracellular signal-regulated kinases (ERK) and p38-MAPK in astrocytes of the spinal dorsal horn. Inhibition of TNF-α or IL-1β ameliorated JNK activation and mechanical allodynia induced by BTZ. Co-administration of thalidomide (TNF-α synthesis inhibitor) and IL-1ra prevented BTZ-induced mechanical allodynia. Conclusion Our results suggest that the TNF-α or IL-1β/JNK pathway in the spinal dorsal horn may play a critical role in the development of painful peripheral neuropathy induced by BTZ., Author(s): Zhen-Yu Li[sup.2] , Yuan-Pei Zhang[sup.1] , Jie Zhang[sup.1] , Su-Bo Zhang[sup.1] , Dai Li[sup.1] , Zhen-Zhen Huang[sup.1] , Wen-Jun Xin[sup.1] Author Affiliations: (1) Department of Physiology and Pain Research [...]

Published
2016
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48. Upregulation of TRPC6 Mediated by PAX6 Hypomethylation Is Involved in the Mechanical Allodynia Induced by Chemotherapeutics in Dorsal Root Ganglion

Author

Zhang, Xiang-Zhong, primary, Luo, De-Xing, primary, Bai, Xiao-Hui, primary, Ding, Huan-Huan, primary, Liu, Meng, primary, Deng, Jie, primary, Mai, Jing-Wen, primary, Yang, Yan-Ling, primary, Zhang, Su-Bo, primary, Ruan, Xiang-Cai, primary, Zhang, Xue-Qin, primary, Xin, Wen-Jun, primary, and Xu, Ting, primary

Published
2020
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