Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function

Claire E. Clarkin; Marwa Mahmoud; Bo Liu; Emmanuel O. Sobamowo; Aileen King; Helen Arthur; Peter M. Jones; Caroline P. Wheeler-Jones

doi:10.1186/s13104-016-2142-z

Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function

Claire E. Clarkin^*, Marwa Mahmoud, Bo Liu, Emmanuel O. Sobamowo, Aileen King, Helen Arthur, Peter M. Jones, Caroline P. Wheeler-Jones

^*Corresponding author for this work

Diabetes

Research output: Contribution to journal › Article › peer-review

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Abstract

Background: Endoglin/CD105 is an auxiliary receptor for transforming growth factor-β with established roles in vascular remodelling. It has recently been shown that heterozygous endoglin deficiency in mice decreases insulin secretion in an animal model of obesity, highlighting a potential role for endoglin in the regulation of islet function. We have previously identified two different populations of endoglin expressing cells in human and mouse islets which are: (i) endothelial cells (ECs) and (ii) islet mesenchymal stromal cells. The contribution of islet EC endoglin expression to islet development and sensitivity to VEGF is unknown and is the focus of this study.

Results: In vitro culture of mouse islets with VEGF₁₆₄ for 48 h increased endoglin mRNA levels above untreated controls but VEGF did not modulate VEGFR2, CD31 or CD34 mRNA expression or islet viability. Removal of EC-endoglin expression in vivo reduced islet EC area but had no apparent effect on islet size or architecture.

Conclusion: EC-specific endoglin expression in islets is sensitive to VEGF and plays partial roles in driving islet vascular development, however such regulation appears to be distinct to mechanisms required to modulate islet viability and size.

Original language	English
Article number	362
Journal	BMC Research Notes
Volume	9
Issue number	1
Early online date	25 Jul 2016
DOIs	https://doi.org/10.1186/s13104-016-2142-z
Publication status	E-pub ahead of print - 25 Jul 2016

Keywords

Endoglin
Hypoxia inducible factor-1 alpha
Islets
VEGF

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1186/s13104-016-2142-zLicence: CC BY

Modulation of endoglin expression_CLARKIN_Accepted 30Jun2016_GOLD VoR
This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
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abstract = "Background: Endoglin/CD105 is an auxiliary receptor for transforming growth factor-β with established roles in vascular remodelling. It has recently been shown that heterozygous endoglin deficiency in mice decreases insulin secretion in an animal model of obesity, highlighting a potential role for endoglin in the regulation of islet function. We have previously identified two different populations of endoglin expressing cells in human and mouse islets which are: (i) endothelial cells (ECs) and (ii) islet mesenchymal stromal cells. The contribution of islet EC endoglin expression to islet development and sensitivity to VEGF is unknown and is the focus of this study. Results: In vitro culture of mouse islets with VEGF164 for 48 h increased endoglin mRNA levels above untreated controls but VEGF did not modulate VEGFR2, CD31 or CD34 mRNA expression or islet viability. Removal of EC-endoglin expression in vivo reduced islet EC area but had no apparent effect on islet size or architecture. Conclusion: EC-specific endoglin expression in islets is sensitive to VEGF and plays partial roles in driving islet vascular development, however such regulation appears to be distinct to mechanisms required to modulate islet viability and size.",

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AU - King, Aileen

AU - Arthur, Helen

AU - Jones, Peter M.

AU - Wheeler-Jones, Caroline P.

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N2 - Background: Endoglin/CD105 is an auxiliary receptor for transforming growth factor-β with established roles in vascular remodelling. It has recently been shown that heterozygous endoglin deficiency in mice decreases insulin secretion in an animal model of obesity, highlighting a potential role for endoglin in the regulation of islet function. We have previously identified two different populations of endoglin expressing cells in human and mouse islets which are: (i) endothelial cells (ECs) and (ii) islet mesenchymal stromal cells. The contribution of islet EC endoglin expression to islet development and sensitivity to VEGF is unknown and is the focus of this study. Results: In vitro culture of mouse islets with VEGF164 for 48 h increased endoglin mRNA levels above untreated controls but VEGF did not modulate VEGFR2, CD31 or CD34 mRNA expression or islet viability. Removal of EC-endoglin expression in vivo reduced islet EC area but had no apparent effect on islet size or architecture. Conclusion: EC-specific endoglin expression in islets is sensitive to VEGF and plays partial roles in driving islet vascular development, however such regulation appears to be distinct to mechanisms required to modulate islet viability and size.

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Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function

Abstract

Keywords

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