# The diagnostic and prognostic value of miR-188-5p in intracranial aneurysm (IA) and its potential regulatory mechanism

**Authors:** Liujia Ma, Lei Shi, Wenjie Tang

PMC · DOI: 10.1186/s41065-025-00593-3 · Hereditas · 2025-11-07

## TL;DR

This study shows that miR-188-5p is a potential biomarker for intracranial aneurysms and may help predict their rupture by affecting vascular smooth muscle cells.

## Contribution

The study identifies miR-188-5p as a novel biomarker for IA diagnosis and progression through its regulatory effects on VSMC phenotypic switching.

## Key findings

- miR-188-5p levels are higher in IA patients and correlate with rupture risk.
- miR-188-5p promotes VSMC dedifferentiation and oxidative stress.
- miR-188-5p negatively regulates IL6ST in VSMCs.

## Abstract

As the etiology of intracranial aneurysm (IA) remains uncertain and unruptured IA management continues to be debated, investigating biomarkers of the disease remains critical. This study thus evaluated the involvement of miR-188-5p in IA diagnosis, prognosis, and development to advance understanding of IA pathophysiology and treatment strategies.

A case-control study involving 73 IA patients and 79 healthy controls was conducted to assess the diagnostic and prognostic value of miR-188-5p in IA. A PDGF-BB-induced VSMC dedifferentiation model was constructed to explore the mechanisms. The qRT-PCR was employed to test the expression of biomolecules, while dual luciferase reporter assays were performed to ensure biomolecule interaction.

The serum expression of miR-188-5p was relatively higher in IA patients than in healthy controls. High serum expression of miR-188-5p exhibited both diagnostic utility for IA detection and predictive capacity for assessing rupture risk. MiR-188-5p inhibited α-SMA and SM22α expression, promoted MMP-2 and MMP-9 expression, and facilitated oxidative stress and proinflammatory cytokine expression in phenotypically switched VSMCs. MiR-188-5p negatively regulated IL6ST expression in phenotypically switched VSMCs. IL6ST mediated the modification of miR-188-5p in phenotypically switched VSMCs.

MiR-188-5p was a biomarker for IA and its rupture. MiR-188-5p might assist IA progression by inducing VSMC phenotypic switching and cell damage. MiR-188-5p affected VSMCs by downregulating IL6ST. MiR-188-5p might be the potential target for predicting and controlling the development of IA.

## Linked entities

- **Genes:** IL6ST (interleukin 6 cytokine family signal transducer) [NCBI Gene 3572], ACTA1 (actin alpha 1, skeletal muscle) [NCBI Gene 58], Tagln (transgelin) [NCBI Gene 21345], MMP2 (matrix metallopeptidase 2) [NCBI Gene 4313], MMP9 (matrix metallopeptidase 9) [NCBI Gene 4318]

## Full-text entities

- **Genes:** TAGLN (transgelin) [NCBI Gene 6876] {aka SM22, SM22-alpha, SMCC, TAGLN1, TGLN, WS3-10}, IL6ST (interleukin 6 cytokine family signal transducer) [NCBI Gene 3572] {aka CD130, CDW130, GP130, HIES4, HIES4A, HIES4B}, ACTA1 (actin alpha 1, skeletal muscle) [NCBI Gene 58] {aka ACTA, ASMA, CFTD, CFTD1, CFTDM, CMYO2A}, MMP2 (matrix metallopeptidase 2) [NCBI Gene 4313] {aka CLG4, CLG4A, MMP-2, MMP-II, MONA, TBE-1}, MMP9 (matrix metallopeptidase 9) [NCBI Gene 4318] {aka CLG4B, GELB, MANDP2, MMP-9}
- **Diseases:** IA (MESH:D002532), rupture (MESH:D012421)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12595658/full.md

## References

16 references — full list in the complete paper: https://tomesphere.com/paper/PMC12595658/full.md

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Source: https://tomesphere.com/paper/PMC12595658