Osteopontin Promotes Angiogenesis in the Spinal Cord and Exerts a Protective Role Against Motor Function Impairment and Neuropathic Pain After Spinal Cord Injury.

Study Design: Basic science study using a hemisection spinal cord injury (SCI) model.

Objective: We sought to assess the effect of blocking osteopontin (OPN) upregulation on motor function recovery and pain behavior after SCI and to further investigate the possible downstream target of OPN in the injured spinal cord.

Summary Of Background Data: OPN is a noncollagenous extracellular matrix protein widely expressed across different tissues.

Upregulation of Spinal miR-155-5p Contributes to Mechanical Hyperalgesia by Promoting Inflammatory Activation of Microglia in Bone Cancer Pain Rats.

Bone cancer pain (BCP) seriously deteriorates the life quality of patients, but its underlying mechanism is still unclear. Spinal microRNAs might contribute to the development of BCP and the role of microglial activation is controversial. In this study, we established a BCP model by injecting Walker 256 breast carcinoma cells into the tibial intramedullary cavity of rats and significant hyperalgesia was observed in the BCP rats.

Analysis of the long non-coding RNA and mRNA expression profiles associated with lidocaine-induced neurotoxicity in the spinal cord of a rat model.

Neurotoxicity is thought to be one of the causes of lidocaine-associated neurological complications; however, the mechanisms underlying lidocaine-related neurotoxicity are still unclear. Long non-coding RNAs (lncRNAs) are novel mediators of neurotoxicity, and their role in lidocaine-induced neurotoxicity needs to be explored. Here, we established a rat model of lidocaine-induced neurotoxicity via the repetitive intrathecal administration of 10% lidocaine.

Ropivacaine represses the proliferation, invasion, and migration of glioblastoma via modulating the microRNA-21-5p/KAT8 regulatory NSL complex subunit 2 axis.

Ropivacaine (Rop) is available to suppress the growth of glioblastoma (GBM), while its mechanism has not been completely elaborated. In this study, we explore the latent mechanism of Rop repressing GBM's growth via mediating the microRNA (miR)-21-5p/KAT8 regulatory NSL complex subunit 2 (KANSL2) axis. MiR-21-5p was declined in GBM, while KANSL2 was elevated.

Downregulation of microRNA-199a-5p alleviated lidocaine-induced sensory dysfunction and spinal cord myelin lesions in a rat model.

Lidocaine induces neurotoxicity in the spinal cord, but the underlying mechanisms remain unclear. In this study, we evaluated the effects of miR-199a-5p on 10 % lidocaine neurotoxicity. Increased expression of miR-199a-5p in the spinal cord of rats treated with 10 % lidocaine was assessed by qRT-PCR.