Losartan inhibits EGFR transactivation in vascular smooth muscle cells


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Kirca M., YEŞİLKAYA A.

TURKISH JOURNAL OF MEDICAL SCIENCES, vol.48, no.6, pp.1364-1371, 2018 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 48 Issue: 6
  • Publication Date: 2018
  • Doi Number: 10.3906/sag-1802-113
  • Journal Name: TURKISH JOURNAL OF MEDICAL SCIENCES
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, TR DİZİN (ULAKBİM)
  • Page Numbers: pp.1364-1371
  • Keywords: Angiotensin II, EGF receptor, losartan, transactivation, extracellular regulated kinase, vascular smooth muscle, cardiovascular disease, EPIDERMAL-GROWTH-FACTOR, FACTOR RECEPTOR TRANSACTIVATION, ANGIOTENSIN-II, ACTIVATION, MECHANISMS, MAPK, ATHEROSCLEROSIS, ALDOSTERONE, LIGANDS, ERK
  • Kütahya Health Sciences University Affiliated: Yes

Abstract

Background/aim: Angiotensin II (Ang II)-induced molecular signaling pathways play a significant role in the progression of cardiovascular diseases, including hypertension and atherosclerosis. In addition to the well-known effects of Ang II, it may activate epidermal growth factor receptor (EGFR) in a process known as transactivation, which contributes to vascular pathologies. The aim of this study was to determine whether losartan could reduce EGFR transactivation induced by Ang II. Additionally, we evaluated the roles of heparin-binding epidermal-like growth factor (HB-EGF) and matrix metalloproteinases (MMPs) in Ang II-induced EGFR transactivation.