miR-188-3p Inhibits Vascular Smooth Muscle Cell Proliferation and Migration by Targeting Fibroblast Growth Factor 1

Shaohua Mi1, Pengfei Wang2, Lejun Lin3

  • 1Department of Cardiology, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, China (mainland).

Insights

MicroRNA-188-3p, a crucial molecule in atherosclerosis, inhibits vascular smooth muscle cell proliferation and migration while promoting apoptosis. This microRNA targets fibroblast growth factor 1 (FGF1), offering potential therapeutic insights for cardiovascular disease.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Biochemistry

Background:

  • Atherosclerosis (AS) is a major cause of cardiovascular disease, linked to vascular smooth muscle cell (VSMC) dysfunction.
  • The precise mechanisms regulating VSMC proliferation and migration in AS require further investigation.

Purpose of the Study:

  • To elucidate the role of miR-188-3p in regulating VSMC behavior.
  • To identify the molecular targets and pathways involved in miR-188-3p's function in AS.

Main Methods:

  • Established AS cell and mouse models using human VSMCs and ApoE-knockout mice.
  • Quantified miR-188-3p and fibroblast growth factor 1 (FGF1) expression via qRT-PCR and Western blot.
  • Assessed VSMC proliferation, migration, and apoptosis using MTT, BrdU, Transwell assays, and flow cytometry.
  • Validated miR-188-3p and FGF1 interaction using dual-luciferase reporter assays.

Main Results:

  • miR-188-3p levels were significantly decreased in AS patients, ApoE-/- mice, and VSMCs exposed to oxidized LDL.
  • miR-188-3p suppressed VSMC proliferation and migration while promoting apoptosis.
  • FGF1 was identified as a direct target gene of miR-188-3p.
  • Restoring FGF1 expression reversed the effects of miR-188-3p on VSMCs.

Conclusions:

  • miR-188-3p acts as a suppressor of VSMC proliferation and migration.
  • miR-188-3p induces VSMC apoptosis by targeting FGF1.
  • This microRNA-target interaction presents a novel mechanism in atherosclerosis development.

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