MiR‐101 promotes pain hypersensitivity in rats with chronic constriction injury via the MKP‐1 mediated MAPK pathway

• Published in: Journal of cellular and molecular medicine Vol. 24; no. 16; pp. 8986 - 8997
• Main Authors: Qiu, Shuang, Liu, Benjuan, Mo, Yanshuai, Wang, Xueqin, Zhong, Lina, Han, Xiao, Mi, Fuli
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01.08.2020; John Wiley and Sons Inc
• Subjects: Animal models; Animals; Binding sites; Catheters; Cell culture; chronic constriction injury; Constriction; Dorsal horn; Dual Specificity Phosphatase 1 - metabolism; Female; Gene expression; Hypersensitivity; Inflammation; Inflammation - metabolism; Interleukin-1beta - metabolism; Intubation; Kinases; Laboratory animals; Latency; Lipopolysaccharides; MAP kinase; Mechanical stimuli; Microglia - metabolism; Microglial cells; MicroRNAs - metabolism; MicroRNA‐101; miRNA; Mitogen-Activated Protein Kinases - metabolism; mitogen‐activated protein kinase phosphatase 1; Nervous system; Neuralgia; Neuralgia - metabolism; NF-kappa B - metabolism; Original; Pain; pain hypersensitivity; Protein kinase; Rats; Rats, Sprague-Dawley; Rodents; Signal transduction; Signal Transduction - physiology; Spinal cord; Spinal Cord - metabolism; spinal cord microglial cell; Surgery; Tumor necrosis factor; Tumor Necrosis Factor-alpha - metabolism; Tumors; chronic constriction injury; mitogen-activated protein kinase phosphatase 1; MicroRNA-101; pain hypersensitivity; spinal cord microglial cell

This study was performed to characterize the effect of microRNA‐101 (miR‐101) on the pain hypersensitivity in CCI rat models with the involvement of mitogen‐activated protein kinase phosphatase 1 (MKP‐1) in spinal cord microglial cells. The mechanical withdrawal threshold (MWT) and thermal withdrawa...