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Losartan inhibits EGFR transactivation in vascular smooth muscle cells

Mustafa Kırça1, Akın Yeşilkaya1

  • 1Department of Biochemistry, School of Medicine, Akdeniz University, Antalya, Turkey

Turkish Journal of Medical Sciences
|December 14, 2018
PubMed
Abstract

Insights

Losartan, an antihypertensive drug, inhibits Angiotensin II-induced EGFR transactivation in vascular cells. This finding suggests EGFR inhibition as a potential therapy for cardiovascular diseases like hypertension.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Pharmacology

Background:

  • Angiotensin II (Ang II) signaling contributes to cardiovascular diseases.
  • Ang II may activate epidermal growth factor receptor (EGFR) via transactivation, promoting vascular pathologies.
  • The roles of HB-EGF and MMPs in Ang II-induced EGFR transactivation require further investigation.

Purpose of the Study:

  • To determine if losartan reduces Ang II-induced EGFR transactivation.
  • To investigate the involvement of heparin-binding epidermal-like growth factor (HB-EGF) and matrix metalloproteinases (MMPs) in this process.

Main Methods:

  • Vascular smooth muscle cells were cultured from rat aortas.
  • Angiotensin II-induced EGFR and ERK1/2 MAPK phosphorylation were assessed using western blotting.

Main Results:

  • Ang II induced EGFR phosphorylation via the Ang II type I receptor (AT1R).
  • Losartan effectively inhibited Ang II-induced EGFR transactivation.
  • This process was mediated by HB-EGF and MMPs, confirming an AT1R-dependent mechanism.

Conclusions:

  • Losartan suppresses EGFR phosphorylation stimulated by Ang II in vascular smooth muscle cells.
  • EGFR inhibition presents a potential therapeutic strategy for hypertension and atherosclerosis.
Keywords:
Angiotensin IIEGF receptorlosartantransactivationextracellular regulated kinasevascular smooth musclecardiovascular disease

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