miRNA-145 is associated with spontaneous hypertension by targeting SLC7A1

Yong Wang1, Liyan Jin2

  • 1Department of General Practice, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.

Insights

MicroRNA-145 (miR-145) is upregulated in hypertension, decreasing nitric oxide. Targeting miR-145 and its downstream SLC7A1 may offer new hypertension treatments.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Hypertension Research

Background:

  • MicroRNAs (miRNAs) are implicated in cardiovascular disease pathogenesis.
  • miR-145 plays a role in various cardiovascular conditions, but its function in hypertension is not fully understood.

Purpose of the Study:

  • To investigate the role of miR-145 in the development of hypertension.
  • To explore the molecular mechanisms underlying miR-145's involvement in hypertension.

Main Methods:

  • Comparison of miR-145 expression in thoracic aorta of spontaneously hypertensive rats (SHR) and control rats.
  • Measurement of nitric oxide (NO) content in SHR and control rats.
  • Silencing miR-145 in rat vascular endothelial cells (RVECs) to assess effects on SLC7A1 and eNOS.
  • Dual-luciferase reporter assay to confirm SLC7A1 as a direct target of miR-145.

Main Results:

  • miR-145 expression was significantly increased in the thoracic aorta of SHR compared to controls.
  • Nitric oxide (NO) content was significantly reduced in SHR.
  • Silencing miR-145 in RVECs led to increased SLC7A1 expression and phosphorylated endothelial nitric oxide synthase (eNOS).
  • SLC7A1 was confirmed as a direct target of miR-145.

Conclusions:

  • miR-145 acts as a key mediator in hypertension pathogenesis by targeting SLC7A1.
  • This interaction affects nitric oxide production and endothelial function.
  • miR-145 represents a potential therapeutic target for hypertension treatment.

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