Mutual Balance between Vasohibin-1 and Soluble VEGFR-1 in Endothelial Cells

Vasohibin-1 (VASH1) is a VEGF-inducible gene of endothelial cells (ECs) that acts as a negative feedback regulator of angiogenesis. To further characterize the function of VASH1, we transfected human VASH1 gene into the mouse EC line MS1, established stable VASH1 expressing clones, and determined ge...

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Main Authors: Miyashita, Hiroki, Suzuki, Hirotada, Ohkuchi, Akihide, Sato, Yasufumi
Format: Online
Language:English
Published: MDPI 2011
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4055955/
id pubmed-4055955
recordtype oai_dc
spelling pubmed-40559552014-06-13 Mutual Balance between Vasohibin-1 and Soluble VEGFR-1 in Endothelial Cells Miyashita, Hiroki Suzuki, Hirotada Ohkuchi, Akihide Sato, Yasufumi Article Vasohibin-1 (VASH1) is a VEGF-inducible gene of endothelial cells (ECs) that acts as a negative feedback regulator of angiogenesis. To further characterize the function of VASH1, we transfected human VASH1 gene into the mouse EC line MS1, established stable VASH1 expressing clones, and determined gene alteration by cDNA microarray analysis. Among the various angiogenesis-related genes, vascular endothelial growth factor type 1 receptor (VEGFR-1) and its alternative spliced form, soluble VEGFR1 (sVEGFR-1), were found to be the most significantly down-regulated genes. Transient overexpression of VASH1 in human umbilical vein endothelial cells confirmed the down-regulation of VEGFR-1 and sVEGFR-1. sVEGFR-1 is a decoy receptor for VEGF and inhibits angiogenesis. Interestingly, when sVEGFR-1 was overexpressed in ECs, it inhibited the expression of VASH1 in turn. These results suggest that VASH1 and sVEGFR-1, two angiogenesis inhibitors, mutually balance their expressions in ECs. MDPI 2011-05-31 /pmc/articles/PMC4055955/ http://dx.doi.org/10.3390/ph4060782 Text en © 2011 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Miyashita, Hiroki
Suzuki, Hirotada
Ohkuchi, Akihide
Sato, Yasufumi
spellingShingle Miyashita, Hiroki
Suzuki, Hirotada
Ohkuchi, Akihide
Sato, Yasufumi
Mutual Balance between Vasohibin-1 and Soluble VEGFR-1 in Endothelial Cells
author_facet Miyashita, Hiroki
Suzuki, Hirotada
Ohkuchi, Akihide
Sato, Yasufumi
author_sort Miyashita, Hiroki
title Mutual Balance between Vasohibin-1 and Soluble VEGFR-1 in Endothelial Cells
title_short Mutual Balance between Vasohibin-1 and Soluble VEGFR-1 in Endothelial Cells
title_full Mutual Balance between Vasohibin-1 and Soluble VEGFR-1 in Endothelial Cells
title_fullStr Mutual Balance between Vasohibin-1 and Soluble VEGFR-1 in Endothelial Cells
title_full_unstemmed Mutual Balance between Vasohibin-1 and Soluble VEGFR-1 in Endothelial Cells
title_sort mutual balance between vasohibin-1 and soluble vegfr-1 in endothelial cells
description Vasohibin-1 (VASH1) is a VEGF-inducible gene of endothelial cells (ECs) that acts as a negative feedback regulator of angiogenesis. To further characterize the function of VASH1, we transfected human VASH1 gene into the mouse EC line MS1, established stable VASH1 expressing clones, and determined gene alteration by cDNA microarray analysis. Among the various angiogenesis-related genes, vascular endothelial growth factor type 1 receptor (VEGFR-1) and its alternative spliced form, soluble VEGFR1 (sVEGFR-1), were found to be the most significantly down-regulated genes. Transient overexpression of VASH1 in human umbilical vein endothelial cells confirmed the down-regulation of VEGFR-1 and sVEGFR-1. sVEGFR-1 is a decoy receptor for VEGF and inhibits angiogenesis. Interestingly, when sVEGFR-1 was overexpressed in ECs, it inhibited the expression of VASH1 in turn. These results suggest that VASH1 and sVEGFR-1, two angiogenesis inhibitors, mutually balance their expressions in ECs.
publisher MDPI
publishDate 2011
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4055955/
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