Background and objectives <p>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.</p> Materials and methods <p>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.</p> Results <p>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.</p> Conclusion <p>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.</p>

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

  • Liujia Ma,
  • Lei Shi,
  • Wenjie Tang

摘要

Background and objectives

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.

Materials and methods

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.

Results

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.

Conclusion

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.