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Hyperglycemia-induced vasculopathy in the murine conceptus is mediated via reductions of VEGF-A expression and VEGF receptor activation

E Pinter, Jody Haigh, A Nagy and JA Madri (2001) AMERICAN JOURNAL OF PATHOLOGY. 158(4). p.1199-1206
abstract
Major congenital malformations, Including those affecting the cardiovascular system, remain the leading cause of mortality and morbidity In infants of diabetic mothers. Interestingly, targeted mutations of several genes (including VEGF and VEGF receptors) and many teratogenic agents (including excess D-glucose) that give rise to embryonic lethal phenotypes during organogenesis are associated with a failure in the formation and/or maintenance of a functional vitelline circulation, Given the similarities in the pathology of the abnormal vitelline circulation in many of these conditions, we hypothesized that the hyperglycemic insult present hn diabetes could cause the resultant abnormalitles in the vitelline circulation by affecting VEGF/VEGF receptor signaling pathway(s). In this study we report that hyperglycemic insult results in reduced levels of VEGF-A in the conceptus, which in turn, leads to abnormal VEGF receptor signaling, ultimately resulting in embryonic (vitelline) vasculopathy. These findings and our observation that addition of exogenous rVEGF-A(165) within a defined concentration range blunts the hyperglycemia-induced vasculopathy in the conceptus support the concept that VEGF levels can be modulated by glucose levels. In addition, these findings may ultimately lead to novel therapeutic approaches for the treatment of selected congenital cardiovascular abnormalities associated with diabetes.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
CELL-ADHESION MOLECULE-1, TYROSINE PHOSPHORYLATION STATE, ENDOTHELIAL GROWTH-FACTOR, IN-VITRO, DIABETIC EMBRYOPATHY, VASCULAR DEVELOPMENT, FLK-1 RECEPTOR, VASCULOGENESIS, FLT-1, DIFFERENTIATION
journal title
AMERICAN JOURNAL OF PATHOLOGY
Am. J. Pathol.
volume
158
issue
4
pages
1199 - 1206
Web of Science type
Article
Web of Science id
000168134000004
JCR category
PATHOLOGY
JCR impact factor
7.103 (2001)
JCR rank
2/66 (2001)
JCR quartile
1 (2001)
ISSN
0002-9440
language
English
UGent publication?
no
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1202135
handle
http://hdl.handle.net/1854/LU-1202135
date created
2011-04-05 11:45:16
date last changed
2016-12-19 15:45:53
@article{1202135,
  abstract     = {Major congenital malformations, Including those affecting the cardiovascular system, remain the leading cause of mortality and morbidity In infants of diabetic mothers. Interestingly, targeted mutations of several genes (including VEGF and VEGF receptors) and many teratogenic agents (including excess D-glucose) that give rise to embryonic lethal phenotypes during organogenesis are associated with a failure in the formation and/or maintenance of a functional vitelline circulation, Given the similarities in the pathology of the abnormal vitelline circulation in many of these conditions, we hypothesized that the hyperglycemic insult present hn diabetes could cause the resultant abnormalitles in the vitelline circulation by affecting VEGF/VEGF receptor signaling pathway(s). In this study we report that hyperglycemic insult results in reduced levels of VEGF-A in the conceptus, which in turn, leads to abnormal VEGF receptor signaling, ultimately resulting in embryonic (vitelline) vasculopathy. These findings and our observation that addition of exogenous rVEGF-A(165) within a defined concentration range blunts the hyperglycemia-induced vasculopathy in the conceptus support the concept that VEGF levels can be modulated by glucose levels. In addition, these findings may ultimately lead to novel therapeutic approaches for the treatment of selected congenital cardiovascular abnormalities associated with diabetes.},
  author       = {Pinter, E and Haigh, Jody and Nagy, A and Madri, JA},
  issn         = {0002-9440},
  journal      = {AMERICAN JOURNAL OF PATHOLOGY},
  keyword      = {CELL-ADHESION MOLECULE-1,TYROSINE PHOSPHORYLATION STATE,ENDOTHELIAL GROWTH-FACTOR,IN-VITRO,DIABETIC EMBRYOPATHY,VASCULAR DEVELOPMENT,FLK-1 RECEPTOR,VASCULOGENESIS,FLT-1,DIFFERENTIATION},
  language     = {eng},
  number       = {4},
  pages        = {1199--1206},
  title        = {Hyperglycemia-induced vasculopathy in the murine conceptus is mediated via reductions of VEGF-A expression and VEGF receptor activation},
  volume       = {158},
  year         = {2001},
}

Chicago
Pinter, E, Jody Haigh, A Nagy, and JA Madri. 2001. “Hyperglycemia-induced Vasculopathy in the Murine Conceptus Is Mediated via Reductions of VEGF-A Expression and VEGF Receptor Activation.” American Journal of Pathology 158 (4): 1199–1206.
APA
Pinter, E., Haigh, J., Nagy, A., & Madri, J. (2001). Hyperglycemia-induced vasculopathy in the murine conceptus is mediated via reductions of VEGF-A expression and VEGF receptor activation. AMERICAN JOURNAL OF PATHOLOGY, 158(4), 1199–1206.
Vancouver
1.
Pinter E, Haigh J, Nagy A, Madri J. Hyperglycemia-induced vasculopathy in the murine conceptus is mediated via reductions of VEGF-A expression and VEGF receptor activation. AMERICAN JOURNAL OF PATHOLOGY. 2001;158(4):1199–206.
MLA
Pinter, E, Jody Haigh, A Nagy, et al. “Hyperglycemia-induced Vasculopathy in the Murine Conceptus Is Mediated via Reductions of VEGF-A Expression and VEGF Receptor Activation.” AMERICAN JOURNAL OF PATHOLOGY 158.4 (2001): 1199–1206. Print.