Overexpression of microRNA-21-5p and microRNA-221-5p in Monocytes Increases the Risk of Developing Coronary Artery

Yazmín Estela Torres-Paz1,2, Ricardo Gamboa1, Giovanny Fuentevilla-Álvarez1,3

  • 1Physiology Department, Instituto Nacional de Cardiología "Ignacio Chávez", México City 14080, Mexico.

Insights

Increased miR-21-5p and miR-221-5p expression in monocytes is linked to higher coronary arterial disease (CAD) risk. Metformin treatment downregulated these microRNAs in CAD patients.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Genetics

Background:

  • MicroRNAs (miRs) are key post-transcriptional regulators of gene expression.
  • Monocytes play a crucial role in cardiovascular health and disease.
  • Specific miRs, including miR-221-5p, miR-21-5p, and miR-155-5p, are implicated in various cellular processes.

Purpose of the Study:

  • To investigate the expression levels of miR-221-5p, miR-21-5p, and miR-155-5p in monocytes.
  • To determine the association of these miRs with coronary arterial disease (CAD) risk.
  • To evaluate the effect of metformin on miR expression in CAD patients.

Main Methods:

  • Quantitative reverse transcription polymerase chain reaction (RT-qPCR) was employed.
  • Monocyte samples were collected from 110 subjects, including healthy controls and CAD patients.
  • Expression levels of miR-221-5p, miR-21-5p, and miR-155-5p were analyzed.

Main Results:

  • miR-21-5p and miR-221-5p showed significantly higher expression in the CAD group (p = 0.001 and p < 0.001, respectively).
  • miR-155-5p expression was significantly lower in the CAD group (p = 0.021).
  • Upregulation of miR-21-5p and miR-221-5p correlated with increased CAD risk; metformin downregulated these miRs in CAD patients.

Conclusions:

  • Overexpression of miR-21-5p and miR-221-5p in monocytes increases CAD risk in Mexican patients.
  • Metformin demonstrates a potential therapeutic role by downregulating miR-21-5p and miR-221-5p.
  • Decreased endothelial nitric oxide synthase (NOS3) expression in CAD patients suggests potential therapeutic targets.

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