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Up-regulation of circulating microRNA-17 is associated with lumbar radicular pain following disc herniation

2019; BioMed Central; Volume: 21; Issue: 1 Linguagem: Inglês

10.1186/s13075-019-1967-y

1478-6362

Eivind Hasvik, Tiril Schjølberg, Daniel Pitz Jacobsen, Anne Julsrud Haugen, Lars Grøvle, Elina Iordanova Schistad, Johannes Gjerstad,

Pregnancy-related medical research

Previous studies suggest that regulatory microRNAs (miRs) may modulate neuro-inflammatory processes. The purpose of the present study was to examine the role of miR-17 following intervertebral disc herniation. In a cohort of 97 patients with leg pain and disc herniation verified on MRI, we investigated the association between circulating miR-17 and leg pain intensity. A rat model was used to examine possible changes in miR-17 expression in nucleus pulposus (NP) associated with leak of NP tissue out of the herniated disc. The functional role of miR-17 was addressed by transfection of miR-17 into THP-1 cells (human monocyte cell line). An association between the level of miR-17 in serum and the intensity of lumbar radicular pain was shown. Up-regulation of miR-17 in the rat NP tissue when applied onto spinal nerve roots and increased release of TNF following transfection of miR-17 into THP-1 cells were also observed. Hence, our data suggest that miR-17 may be involved in the pathophysiology underlying lumbar radicular pain after disc herniation. We conclude that miR-17 may be associated with the intensity of lumbar radicular pain after disc herniation, possibly through a TNF-driven pro-inflammatory mechanism.