2009
Characterization of RAGE, HMGB1, and S100β in Inflammation-Induced Preterm Birth and Fetal Tissue Injury
Buhimschi CS, Baumbusch MA, Dulay AT, Oliver EA, Lee S, Zhao G, Bhandari V, Ehrenkranz RA, Weiner CP, Madri JA, Buhimschi IA. Characterization of RAGE, HMGB1, and S100β in Inflammation-Induced Preterm Birth and Fetal Tissue Injury. American Journal Of Pathology 2009, 175: 958-975. PMID: 19679874, PMCID: PMC2731116, DOI: 10.2353/ajpath.2009.090156.Peer-Reviewed Original ResearchConceptsDamage-associated molecular pattern moleculesMolecular pattern moleculesPreterm birthTissue injuryPattern moleculesInflammation-induced preterm birthBiology of RAGEExpression of RAGERole of RAGERobust inflammatory responseRelease of HMGB1Fetal inflammationFetal injuryFetal circulationFetal damageImmune activationInterleukin-6Inflammatory responseAdvanced glycationAnimal modelsCellular injuryHuman fetusesTissue damageS100 proteinInjury
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
1994
Extracellular Matrix‐Degrading Proteinases in the Nervous System
Romanic A, Madri J. Extracellular Matrix‐Degrading Proteinases in the Nervous System. Brain Pathology 1994, 4: 145-156. PMID: 8061860, DOI: 10.1111/j.1750-3639.1994.tb00825.x.Peer-Reviewed Original ResearchConceptsCell-ECM interactionsExtracellular matrixMatrix-degrading proteinasesNeuronal cell migrationExtracellular matrix-degrading proteinasesCell migrationNervous systemECM degradationNeurite outgrowthCell proliferationDrug designProteolytic activityNew insightsPathological conditionsBrain tumor growthTumor growthMatrix metalloproteinasesProteinasesForm of therapyCentral nervous systemInhibitorsPlasminogen activatorTraffickingLeukocyte traffickingNerve demyelination
1986
Collagen types I, III, and V in human embryonic and fetal skin
Smith L, Holbrook K, Madri J. Collagen types I, III, and V in human embryonic and fetal skin. Developmental Dynamics 1986, 175: 507-521. PMID: 3521252, DOI: 10.1002/aja.1001750409.Peer-Reviewed Original ResearchConceptsDermal-epidermal junctionReticular regionsType IIIFetal skinType IType VCollagen type IWeeks of gestationSubdermal connective tissueAdult-like patternLarge diameter fibrilsGestational ageFirst trimesterImmunoperoxidase dataPapillary regionImmunoperoxidase stainingType III collagenFetal ageFibrillar collagenLight microscope levelBlood vesselsConnective tissueDermal collagen fibrilsCollagen fibrilsType V collagen