1994
Exposure of Endothelial Cells to Cyclic Strain Induces c-fos, fosB and c-jun But not jun B or jun D and Increases the Transcription Factor AP-1
Sumpio B, Du W, Xu W. Exposure of Endothelial Cells to Cyclic Strain Induces c-fos, fosB and c-jun But not jun B or jun D and Increases the Transcription Factor AP-1. Endothelium 1994, 2: 149-156. DOI: 10.3109/10623329409088469.Peer-Reviewed Original ResearchActivator protein-1Gel shiftHuman umbilical vein ECTranscriptional activator AP-1Fos family genesTranscription factor AP-1Intracellular regulatory eventsC-jun geneFactor AP-1Protein kinase CC-fosFamily genesSteady-state levelsActivation of PKCNuclear proteinsRegulatory eventsJun genesExpression of JUNGene expressionKinase CC-JunNorthern blotEndothelial cell proliferationDownstream inductionGenes
1992
Protein kinase C is a mediator of the adaptation of vascular endothelial cells to cyclic strain in vitro.
Rosales OR, Sumpio BE. Protein kinase C is a mediator of the adaptation of vascular endothelial cells to cyclic strain in vitro. Surgery 1992, 112: 459-66. PMID: 1379381.Peer-Reviewed Original ResearchConceptsProtein kinase CActivation of PKCImmunocytochemical stainingPKC activityCyclic stretchEndothelial cell activationVascular endothelial cellsCycles/minSustained elevationCell activationFlexible-bottomed culture platesKinase CBovine aortic ECsECS resultsEndothelial cellsBlood vesselsAortic ECsEvidence of translocationSpecific PKC inhibitorEC proliferationCalphostin CEC growthHemodynamic forces