2003
Maternal Diabetes: Effects on Embryonic Vascular Development—A Vascular Endothelial Growth Factor-A-mediated Process
Madri JA, Enciso J, Pinter E. Maternal Diabetes: Effects on Embryonic Vascular Development—A Vascular Endothelial Growth Factor-A-mediated Process. Pediatric And Developmental Pathology 2003, 6: 334-341. PMID: 14692647, DOI: 10.1007/s10024-003-5051-9.Peer-Reviewed Original ResearchConceptsEmbryonic lethal phenotypeGrowth factorVascular endothelial growth factorEndothelial growth factorEpithelial-mesenchymal transformationCardiovascular patterningAberrant organogenesisLethal phenotypeVasculogenesis/angiogenesisPhosphorylation stateTargeted mutationsYolk sacMajor congenital malformationsFactor 1Major birth defectsGrowth factor-1OrganogenesisAdhesion moleculesConceptus culturesMaternal diabetesDiabetic miceCardiovascular abnormalitiesVitelline circulationCongenital malformationsBirth defects
2001
Hyperglycemia-Induced Vasculopathy in the Murine Conceptus Is Mediated via Reductions of VEGF-A Expression and VEGF Receptor Activation
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: 1199-1206. PMID: 11290536, PMCID: PMC1891927, DOI: 10.1016/s0002-9440(10)64069-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlood VesselsEndothelial Growth FactorsFetal DiseasesFetusHyperglycemiaLymphokinesMicePhosphorylationReceptor Protein-Tyrosine KinasesReceptors, Growth FactorReceptors, Vascular Endothelial Growth FactorTime FactorsVascular DiseasesVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsVEGF receptorsMajor congenital malformationsCongenital cardiovascular abnormalitiesVEGF/VEGF receptorVitelline circulationNovel therapeutic approachesLevels of VEGFReduction of VEGFCause of mortalityDiabetic mothersInsult resultsVEGF levelsCardiovascular abnormalitiesHyperglycemic insultGlucose levelsTherapeutic approachesCongenital malformationsResultant abnormalitiesReceptor activationVEGF receptor activationCardiovascular systemTeratogenic agentsVasculopathyDiabetesConceptus
1999
Hyperglycemia-Induced Vasculopathy in the Murine Vitelline Vasculature Correlation with PECAM-1/CD31 Tyrosine Phosphorylation State
Pinter E, Mahooti S, Wang Y, Imhof B, Madri J. Hyperglycemia-Induced Vasculopathy in the Murine Vitelline Vasculature Correlation with PECAM-1/CD31 Tyrosine Phosphorylation State. American Journal Of Pathology 1999, 154: 1367-1379. PMID: 10329590, PMCID: PMC1866605, DOI: 10.1016/s0002-9440(10)65391-6.Peer-Reviewed Original ResearchConceptsPECAM-1 tyrosine phosphorylationTyrosine phosphorylation stateMurine conceptusYolk sacCell-extracellular matrixFirst organ systemCell-factor interactionsTyrosine dephosphorylationEndothelial cell migrationEmbryonic angioblastsEmbryonic developmentMesodermal cellsVasculogenesis/angiogenesisTyrosine phosphorylationPhosphorylation statePerinatal lethalityNormal organogenesisVascular systemCell migrationHematopoietic cellsDiabetic pregnant miceComplex vascular systemVasculogenesisPECAM-1 expressionOffspring