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Inhibitory effects of vasostatin-1 against atherogenesis

Yuki Sato1, Rena Watanabe1, Nozomi Uchiyama1

  • 1Laboratory of Cardiovascular Medicine, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.

Clinical Science (London, England : 1979)
|November 8, 2018
PubMed

Insights

This study shows vasostatin-1 inhibits key processes in atherosclerosis development, including inflammation and foam cell formation. Vasostatin-1 administration reduced atherosclerotic lesions in mice, suggesting its therapeutic potential for this cardiovascular disease.

Area of Science:

  • Cardiovascular Science
  • Molecular Biology
  • Immunology

Background:

  • Vasostatin-1, a peptide derived from chromogranin A, is known to inhibit vasoconstriction and angiogenesis.
  • Previous research indicated vasostatin-1 reduces monocyte adhesion to endothelial cells by down-regulating adhesion molecules.

Purpose of the Study:

  • To investigate vasostatin-1 expression in human atherosclerotic lesions.
  • To evaluate vasostatin-1's effects on inflammatory responses, macrophage foam cell formation, smooth muscle cell behavior, and extracellular matrix production.
  • To assess vasostatin-1's impact on atherogenesis in apolipoprotein E-deficient (ApoE-/-) mice.

Main Methods:

  • Vasostatin-1 expression analysis in human radial arteries.
  • In vitro studies on human endothelial cells (HECs) and THP-1 derived macrophages assessing inflammatory markers (MCP-1, VCAM-1, E-selectin, IL-6) and M1 phenotype.
  • Macrophage foam cell formation assays involving oxLDL, ACAT-1, CD36, and ABCA1.
  • Human aortic smooth muscle cell (HASMC) assays for migration, proliferation, apoptosis, and ECM production (collagen-3, fibronectin, elastin, MMP-2, MMP-9) with AngII stimulation.
  • In vivo study using ApoE-/- mice with chronic vasostatin-1 infusion.

Main Results:

  • Vasostatin-1 was detected in human atherosclerotic lesions.
  • Vasostatin-1 suppressed LPS-induced inflammatory responses in HECs and macrophages, including MCP-1, VCAM-1, E-selectin, IL-6, and M1 phenotype via NF-κB down-regulation.
  • Vasostatin-1 inhibited oxLDL-induced foam cell formation by modulating ACAT-1, CD36, and ABCA1.
  • In HASMCs, vasostatin-1 reduced AngII-induced migration and collagen/fibronectin expression (via ERK1/2, p38 inhibition) but increased elastin and MMPs (via Akt, JNK activation).
  • Vasostatin-1 did not affect HASMC proliferation or apoptosis.
  • ApoE-/- mice treated with vasostatin-1 showed reduced aortic atherosclerotic lesions, inflammation, macrophage infiltration, SMC content, and plasma glucose levels.

Conclusions:

  • Vasostatin-1 exhibits significant inhibitory effects against multiple facets of atherogenesis.
  • The findings suggest vasostatin-1 has potential as a novel therapeutic target for atherosclerosis.
  • Vasostatin-1 demonstrates pleiotropic anti-atherogenic properties, impacting inflammation, lipid metabolism, and vascular remodeling.

Keywords:
atherosclerosisendothelial cellmacrophagevascular smooth muscle cellvasostatin-1

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