Low-Power Lasers Therapy Induced Mir-143 Upregulation: A Novel Biomarker and Therapeutic Strategy for Restenosis

Coronary artery disease (CAD) remains a leading global cause of mortality, with percutaneous coronary intervention (PCI) being a primary treatment. However, in-stent restenosis (ISR) affects 15%-30% of cases, driven by vascular injury, inflammation, and smooth muscle cell proliferation. While drug-eluting stents reduce ISR rates, late complications persist. Low-level laser therapy (LLLT) has emerged as a potential adjunctive treatment, modulating inflammation and cell behavior, but its effects on endothelial cells miRNA regulation remain unclear.

This study investigated LLLT's impact on human umbilical vein endothelial cell (HUVEC) migration, proliferation, and miR-143 expression, a key regulator and potential biomarker in vascular restenosis.

HUVECs were cultured and exposed to 532 and 633 nm lasers at varying durations (10-200 s). Cell migration was assessed via scratch wound assays, with imaging at 1, 5-, 12-, 24-, and 48-h post-irradiation. Proliferation and viability were quantified using image analysis (MATLAB). For gene expression, irradiated cells were incubated for 24 h, followed by RNA extraction, cDNA synthesis, and qRT-PCR to measure miR-143 levels.

The 532 nm laser inhibited HUVEC migration most effectively at 10 s, minimizing cytotoxicity. In contrast, the 633 nm laser required longer exposure (200 s) for comparable inhibition but induced delayed miR-143 upregulation after 24 h, suggesting epigenetic modulation. Both wavelengths influenced cell behavior in a time- and dose-dependent manner, with 532 nm offering rapid effects and 633 nm potentially exerting longer-term genetic regulation.

LLLT at specific wavelengths differentially modulates endothelial cell migration and miR-143 expression, highlighting its potential as a non-invasive strategy to mitigate restenosis. The 532 nm laser provides immediate anti-migratory effects, while 633 nm may offer sustained benefits via miRNA regulation. Further research should optimize parameters and validate these findings in vivo to advance LLLT as a complementary therapy for vascular interventions.