Regulatory function of HSA-miR-186-5p on interleukin-2 expression in lumbar degenerative disc disease: a case-control study and subgroups analysis

TL;DR

This study explores how HSA-miR-186-5p and interleukin-2 are linked in lumbar degenerative disc disease, suggesting they could be important biomarkers for disease progression and treatment.

Contribution

The study identifies a novel regulatory relationship between HSA-miR-186-5p and IL-2 in LDDD, particularly in early and moderate disease stages.

Findings

LDDD patients had significantly higher IL-2 levels compared to healthy controls.

miR-186-5p expression was significantly reduced in LDDD patients.

An inverse correlation between IL-2 and miR-186-5p levels was observed across disease subgroups.

Abstract

Lumbar degenerative disc disease (LDDD) is characterized by persistent inflammation and extracellular matrix degradation. Emerging as main controllers in its pathogenesis are microRNAs (miRNAs) and proinflammatory cytokines. Through the JAK/STAT signalling pathway, HSA-miR-186-5p has been linked to modulating cytokine expression, including interleukin-2 (IL-2). The aim is to find the expression levels of IL-2 and HSA-miR-186-5p in LDDDpatients and investigate their possible correlation with disease degree. 110 LDDD patients and 17 healthy controls wereincluded. ELISA measured serum IL-2 concentrations, and RT-qPCRestimated miR-186-5p levels. The Oswestry Disability Index (ODI) guidedpatients into five subgroups (G1–G5). One-way ANOVA and correlationanalysis were applied in statistical comparisons. LDDD patients had notably higher IL-2 levels than controls (p <0.001). According to the subgroup analysis, the IL-2 concentration peaked inG2 and G3 and gradually dropped toward G5. By contrast, miR-186-5pexpression was noticeably lowered in the LDDD group (p < 0.001), with G1and G5 having the lowest levels found. Across groups, an inverse trend in IL-2 and miR-186-5p expression was noted. Results imply a dysregulated interaction between HSA-miR-186-5p and IL-2 in LDDD. Particularly in early and moderate stages ofdisease, miR-186-5p downregulation could help to explain increased IL-2-mediated inflammation. These biomarkers could provide information ondisease activity and present targets for new treatments.

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