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Isolation of Human Umbilical Vein Endothelial Cells HUVEC
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Effect of Angiotensin II on Matrix Metalloproteinase-2 Secretion in Human Umbilical Vein Endothelial Cells

Ryo Sato1,2,3, Chika Hiraishi2,3, Hiroshi Yoshida1,2,3,4

  • 1Department of Laboratory Medicine, The Jikei University Kashiwa Hospital, Chiba, Japan.

Journal of Cardiovascular Pharmacology
|January 26, 2018
PubMed

Insights

Angiotensin II (Ang-II) increases matrix metalloproteinase-2 (MMP-2) in endothelial cells, primarily via AT2 receptors. This finding may offer new insights into cardiovascular disease mechanisms and potential therapeutic targets.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Endothelial Cell Biology

Background:

  • Matrix metalloproteinases (MMPs), particularly MMP-2, are implicated in atherosclerotic plaque destabilization and rupture.
  • Angiotensin II (Ang-II) is a key mediator in cardiovascular disease progression, influencing atherosclerosis and cardiac hypertrophy.
  • Endothelial cells play a crucial role in vascular health and disease, including the regulation of MMPs.

Purpose of the Study:

  • To investigate the regulatory role of Angiotensin II (Ang-II) on MMP-2 expression and secretion in human umbilical vein endothelial cells (HUVECs).
  • To determine the specific Angiotensin II receptor subtypes (AT1 or AT2) involved in mediating the effects of Ang-II on MMP-2 in HUVECs.

Main Methods:

  • HUVECs were treated with Ang-II to assess its impact on MMP-2 secretion and messenger RNA (mRNA) expression.
  • The effects of Ang-II were evaluated in the presence of specific blockers for Ang-II receptor type 1 (AT1 receptor; telmisartan) and Ang-II receptor type 2 (AT2 receptor; PD123319).

Main Results:

  • Ang-II significantly upregulated both MMP-2 secretion and MMP-2 mRNA expression in HUVECs.
  • Co-administration of telmisartan (AT1 blocker) or PD123319 (AT2 blocker) suppressed the Ang-II-induced increase in MMP-2.
  • PD123319 demonstrated a more pronounced suppression of Ang-II's effect on MMP-2, suggesting a dominant role for AT2 receptors.

Conclusions:

  • Angiotensin II enhances MMP-2 production in endothelial cells predominantly through the activation of AT2 receptors.
  • While both AT1 and AT2 receptors are present in HUVECs, the AT2 receptor appears to be the primary mediator of Ang-II's effect on MMP-2.
  • Further clinical studies are needed to confirm the significance of circulating MMP-2 as a cardiovascular biomarker.

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