0000000000849123

AUTHOR

Hannes C.a. Drexler

showing 2 related works from this author

Microphthalmia, persistent hyperplastic hyaloid vasculature and lens anomalies following overexpression of VEGF-A188 from the αA-crystallin promoter

2007

Purpose During growth of the embryonic eye, dose- and site-specific expression of heparin-binding growth factors is critical for the formation of an appropriate vascular supply. Overexpression of vascular endothelial growth factor-A188 (VEGF-A188), a strongly heparin-binding, endothelial-specific mitogen, leads to severe disturbance of vascular and overall ocular morphology. This study aimed to evaluate the effects of VEGF-A188 overexpression on growth of ocular tissue components. Methods Stereological and immunohistochemical methods were employed to identify the vascular profiles, ocular tissue proportions, and cell types in VEGF-A188 transgenic mice and compare them with wild-type mice. R…

Vascular Endothelial Growth Factor Agenetic structuresMyocytes Smooth MuscleCell CountMice TransgenicEyealpha-Crystallin A ChainCongenital AbnormalitiesCorneaMiceLens CrystallineAnimalsMicrophthalmosVascular DiseasesPromoter Regions GeneticHyperplasiaEndothelial CellsHypertrophyEmbryo MammalianAntigens DifferentiationImmunohistochemistryeye diseasesActinsDisease Models AnimalAnimals NewbornBlood Vesselssense organsPericytesHeparan Sulfate ProteoglycansResearch ArticleMolecular Vision
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Inhibition of proteasome function induces programmed cell death in proliferating endothelial cells.

2000

Proteolysis mediated by the ubiquitin-proteasome system has been implicated in the regulation of programmed cell death. Here we investigated the differential effects of proteasomal inhibitors on the viability of proliferating and quiescent primary endothelial cells in vitro and in vivo. Subconfluent, proliferating cells underwent carbobenzoxy-L-isoleucyl-gamma-t-butyl-L-glutamyl-L-alanyl-L-leucinal (PSI) -induced apoptosis at low concentrations (EC(50)=24 nM), whereas at least 340-fold higher concentrations of PSI were necessary to obtain the same effect in confluent, contact-inhibited cells. PSI-mediated cell death could be blocked by a caspase-3 inhibitor (Ac-DEVD-H), but not by a caspase…

Programmed cell deathProteasome Endopeptidase ComplexAngiogenesisProteolysisApoptosisChick EmbryoCysteine Proteinase InhibitorsBiochemistryDogsMultienzyme ComplexesGeneticsmedicineAnimalsHumansMolecular BiologyCells Culturedmedicine.diagnostic_testChemistryCell cycleDifferential effectsCell biologyCysteine EndopeptidasesProteasomeCattleEndothelium VascularFunction (biology)Cell DivisionBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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