Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function
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 en...
Ausführliche Beschreibung
Autor*in: |
Clarkin, Claire E. [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2016 |
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Anmerkung: |
© The Author(s) 2016 |
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Übergeordnetes Werk: |
Enthalten in: BMC Research Notes - London, 2008, 9(2016), 1 vom: 25. Juli |
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Übergeordnetes Werk: |
volume:9 ; year:2016 ; number:1 ; day:25 ; month:07 |
Links: |
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DOI / URN: |
10.1186/s13104-016-2142-z |
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Katalog-ID: |
SPR030317258 |
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520 | |a 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 $ VEGF_{164} $ 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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700 | 1 | |a Sobamowo, Emmanuel O. |4 aut | |
700 | 1 | |a King, Aileen |4 aut | |
700 | 1 | |a Arthur, Helen |4 aut | |
700 | 1 | |a Jones, Peter M. |4 aut | |
700 | 1 | |a Wheeler-Jones, Caroline P. |4 aut | |
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10.1186/s13104-016-2142-z doi (DE-627)SPR030317258 (SPR)s13104-016-2142-z-e DE-627 ger DE-627 rakwb eng Clarkin, Claire E. verfasserin (orcid)0000-0001-6859-5897 aut Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 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 $ VEGF_{164} $ 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. Islets (dpeaa)DE-He213 Endoglin (dpeaa)DE-He213 VEGF (dpeaa)DE-He213 Hypoxia inducible factor-1 alpha (dpeaa)DE-He213 Mahmoud, Marwa aut Liu, Bo aut Sobamowo, Emmanuel O. aut King, Aileen aut Arthur, Helen aut Jones, Peter M. aut Wheeler-Jones, Caroline P. aut Enthalten in BMC Research Notes London, 2008 9(2016), 1 vom: 25. Juli (DE-627)559431805 (DE-600)2413336-X 1756-0500 nnns volume:9 year:2016 number:1 day:25 month:07 https://dx.doi.org/10.1186/s13104-016-2142-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2016 1 25 07 |
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10.1186/s13104-016-2142-z doi (DE-627)SPR030317258 (SPR)s13104-016-2142-z-e DE-627 ger DE-627 rakwb eng Clarkin, Claire E. verfasserin (orcid)0000-0001-6859-5897 aut Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 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 $ VEGF_{164} $ 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. Islets (dpeaa)DE-He213 Endoglin (dpeaa)DE-He213 VEGF (dpeaa)DE-He213 Hypoxia inducible factor-1 alpha (dpeaa)DE-He213 Mahmoud, Marwa aut Liu, Bo aut Sobamowo, Emmanuel O. aut King, Aileen aut Arthur, Helen aut Jones, Peter M. aut Wheeler-Jones, Caroline P. aut Enthalten in BMC Research Notes London, 2008 9(2016), 1 vom: 25. Juli (DE-627)559431805 (DE-600)2413336-X 1756-0500 nnns volume:9 year:2016 number:1 day:25 month:07 https://dx.doi.org/10.1186/s13104-016-2142-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2016 1 25 07 |
allfields_unstemmed |
10.1186/s13104-016-2142-z doi (DE-627)SPR030317258 (SPR)s13104-016-2142-z-e DE-627 ger DE-627 rakwb eng Clarkin, Claire E. verfasserin (orcid)0000-0001-6859-5897 aut Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 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 $ VEGF_{164} $ 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. Islets (dpeaa)DE-He213 Endoglin (dpeaa)DE-He213 VEGF (dpeaa)DE-He213 Hypoxia inducible factor-1 alpha (dpeaa)DE-He213 Mahmoud, Marwa aut Liu, Bo aut Sobamowo, Emmanuel O. aut King, Aileen aut Arthur, Helen aut Jones, Peter M. aut Wheeler-Jones, Caroline P. aut Enthalten in BMC Research Notes London, 2008 9(2016), 1 vom: 25. Juli (DE-627)559431805 (DE-600)2413336-X 1756-0500 nnns volume:9 year:2016 number:1 day:25 month:07 https://dx.doi.org/10.1186/s13104-016-2142-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2016 1 25 07 |
allfieldsGer |
10.1186/s13104-016-2142-z doi (DE-627)SPR030317258 (SPR)s13104-016-2142-z-e DE-627 ger DE-627 rakwb eng Clarkin, Claire E. verfasserin (orcid)0000-0001-6859-5897 aut Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 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 $ VEGF_{164} $ 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. Islets (dpeaa)DE-He213 Endoglin (dpeaa)DE-He213 VEGF (dpeaa)DE-He213 Hypoxia inducible factor-1 alpha (dpeaa)DE-He213 Mahmoud, Marwa aut Liu, Bo aut Sobamowo, Emmanuel O. aut King, Aileen aut Arthur, Helen aut Jones, Peter M. aut Wheeler-Jones, Caroline P. aut Enthalten in BMC Research Notes London, 2008 9(2016), 1 vom: 25. Juli (DE-627)559431805 (DE-600)2413336-X 1756-0500 nnns volume:9 year:2016 number:1 day:25 month:07 https://dx.doi.org/10.1186/s13104-016-2142-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2016 1 25 07 |
allfieldsSound |
10.1186/s13104-016-2142-z doi (DE-627)SPR030317258 (SPR)s13104-016-2142-z-e DE-627 ger DE-627 rakwb eng Clarkin, Claire E. verfasserin (orcid)0000-0001-6859-5897 aut Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 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 $ VEGF_{164} $ 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. Islets (dpeaa)DE-He213 Endoglin (dpeaa)DE-He213 VEGF (dpeaa)DE-He213 Hypoxia inducible factor-1 alpha (dpeaa)DE-He213 Mahmoud, Marwa aut Liu, Bo aut Sobamowo, Emmanuel O. aut King, Aileen aut Arthur, Helen aut Jones, Peter M. aut Wheeler-Jones, Caroline P. aut Enthalten in BMC Research Notes London, 2008 9(2016), 1 vom: 25. Juli (DE-627)559431805 (DE-600)2413336-X 1756-0500 nnns volume:9 year:2016 number:1 day:25 month:07 https://dx.doi.org/10.1186/s13104-016-2142-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2016 1 25 07 |
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Clarkin, Claire E. misc Islets misc Endoglin misc VEGF misc Hypoxia inducible factor-1 alpha Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function |
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Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function Islets (dpeaa)DE-He213 Endoglin (dpeaa)DE-He213 VEGF (dpeaa)DE-He213 Hypoxia inducible factor-1 alpha (dpeaa)DE-He213 |
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Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function |
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Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function |
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Clarkin, Claire E. Mahmoud, Marwa Liu, Bo Sobamowo, Emmanuel O. King, Aileen Arthur, Helen Jones, Peter M. Wheeler-Jones, Caroline P. |
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modulation of endoglin expression in islets of langerhans by vegf reveals a novel regulator of islet endothelial cell function |
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Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function |
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 $ VEGF_{164} $ 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. © The Author(s) 2016 |
abstractGer |
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 $ VEGF_{164} $ 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. © The Author(s) 2016 |
abstract_unstemmed |
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 $ VEGF_{164} $ 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. © The Author(s) 2016 |
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Modulation of endoglin expression in islets of langerhans by VEGF reveals a novel regulator of islet endothelial cell function |
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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 $ VEGF_{164} $ 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. 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