J Lipid Atheroscler.  2016 Dec;5(2):107-113. 10.12997/jla.2016.5.2.107.

Novel Molecular Basis for Vascular Health Regulated by Vasohibin-1

Affiliations
  • 1Department of Vascular Biology, Institute of Development, Aging and Cancer, Tohoku University, Japan. yasufumi.sato.b3@tohoku.ac.jp

Abstract

The endothelium covers the entire luminal surface of blood vessels, organizes the interface between the blood and underlying tissues, and controls vascular tone, blood clotting, transport of various substances across the vascular wall, adhesion and transmigration of leukocytes, and so forth. The structural and functional integrity of endothelium is essential for the maintenance of vascular health. In light of its important role, the endothelium should have a self-defense system such as vasohibin-1 (VASH1), a protein preferentially expressed in endothelial cells (ECs). Unique features of VASH1 are its anti-angiogenic activity and ability to promote stress tolerance of ECs. This mini review summarizes the current understanding of VASH1, especially the posttranscriptional regulation of its synthesis in response to cellular stresses and aging.

Keyword

Vasohibin-1; Endothelial cell; Anti-angiogenesis; Stress tolerance; Gene regulation

MeSH Terms

Aging
Blood Coagulation
Blood Vessels
Endothelial Cells
Endothelium
Leukocytes
Phenobarbital
Phenobarbital

Figure

  • Fig. 1 The regulation of vasohibin-1 (VASH1) synthesis in response to angiogenic stimuli, cellular stresses and aging: VASH1 is transcriptionally induced in ECs by angiogenic stimuli and inhibits angiogenesis as a negative-feedback regulator. In addition, the synthesis of VASH1 receives post-transcriptional regulation. Cellular stresses increase the synthesis of VASH1 via HuR for stress tolerance. In contrast, replicative senescence of endothelial cells (ECs) decreases the synthesis of VASH1 via miR-22, and this might be one of the causes of age-related vascular diseases.


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