Decreased miR-325-5p Contributes to Visceral Hypersensitivity Through Post-transcriptional Upregulation of CCL2 in Rat Dorsal Root Ganglia

【Author】

Rui Wu;Ping-An Zhang;Xuelian Liu;Yuan Zhou;Meijie Xu;Xinghong Jiang;Jun Yan;Guang-Yin Xu;Center for Translational Medicine, Affiliated Zhangjiagang Hospital of Soochow University;Department of Physiology and Neurobiology, Institute of Neuroscience, Soochow University;The Second Affiliated of Hospital Soochow University;

【Institution】

Center for Translational Medicine, Affiliated Zhangjiagang Hospital of Soochow University;Department of Physiology and Neurobiology, Institute of Neuroscience, Soochow University;The Second Affiliated of Hospital Soochow University;

【Abstract】

Chronic visceral hypersensitivity is an important type of chronic pain with unknown etiology and pathophysiology. Recent studies have shown that epigenetic regulation plays an important role in the development of chronic pain conditions. However, the role of mi RNA-325-5 p in chronic visceral pain remains unknown. The present study was designed to determine the roles and mechanism of mi RNA-325-5 p in a rat model of chronic visceral pain.This model was induced by neonatal colonic inflammation(NCI). In adulthood, NCI led to a significant reduction in the expression of mi RNA-325-5 p in colon-related dorsal root ganglia(DRGs), starting to decrease at the age of4 weeks and being maintained to 8 weeks. Intrathecal administration of mi RNA-325-5 p agomir significantly enhanced the colorectal distention(CRD) threshold in a time-dependent manner. NCI also markedly increased the expression of CCL2(C-C motif chemokine ligand 2) in colon-related DRGs at the m RNA and protein levels relative to age-matched control rats. The expression of CXCL12, IL33, SFRS7, and LGI1 was not significantlyaltered in NCI rats. CCL2 was co-expressed in Neu Npositive DRG neurons but not in glutamine synthetasepositive glial cells. Furthermore, CCL2 was mainly expressed in isolectin B4-binding-and calcitonin generelated peptide-positive DRG neurons but in few NF-200-positive cells. More importantly, CCL2 was expressed in mi R-325-5 p-positive DRG neurons. Intrathecal injection of mi RNA-325-5 p agomir remarkably reduced the upregulation of CCL2 in NCI rats. Administration of Bindarit, an inhibitor of CCL2, markedly raised the CRD threshold in NCI rats in a dose-and time-dependent manner. These data suggest that NCI suppresses mi RNA-325-5 p expression and enhances CCL2 expression, thus contributing to visceral hypersensitivity in adult rats.

【Keywords】

Visceral pain;;Dorsal root ganglia;;miRNA-325-5p;;CCL2;;Epigenetic regulation

References

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Springer Journals Database

Total: 18 articles

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  • [3] Rou-Gang Xie;Yong-Jing Gao;Chul-Kyu Park;Ning Lu;Ceng Luo;Wen-Ting Wang;Sheng-Xi Wu;Ru-Rong Ji;Department of Neurobiology and Collaborative Innovation Center for Brain Science, The Fourth Military Medical University;Department of Anesthesiology, Duke University Medical Center;Pain Research Laboratory, Institute of Nautical Medicine Jiangsu Key laboratory of Neuroregeneration, Nantong University;Department of Physiology, College of Medicine, Gachon University;Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University;Department of Neurobiology, Duke University Medical Center;, Spinal CCL2 Promotes Central Sensitization, Long-Term Potentiation,and Inflammatory Pain via CCR2:Further Insights into Molecular,Synaptic,and Cellular Mechanisms, Neuroscience Bulletin,
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