6533b832fe1ef96bd129aebd

RESEARCH PRODUCT

Tumorigenic conversion of endothelial cells.

C. James KirkpatrickUlrich KlotzVera Krump-konvalinkovaElke KleideiterUlrike Friedrich

subject

CD31AdultLipopolysaccharidesTelomerasePathologymedicine.medical_specialtyClinical BiochemistryCaveolin 1Vascular Cell Adhesion Molecule-1BiologyCaveolinsPathology and Forensic Medicinevon Willebrand FactormedicineCell AdhesionHumansMolecular BiologyTelomeraseCells CulturedCell NucleusCell adhesion moleculeReverse Transcriptase Polymerase Chain ReactionGranulocyte-Macrophage Colony-Stimulating FactorTelomereIntercellular Adhesion Molecule-1Cell biologyVascular endothelial growth factor BEndothelial stem cellDNA-Binding ProteinsPlatelet Endothelial Cell Adhesion Molecule-1Vascular endothelial growth factor ACell Transformation NeoplasticVascular endothelial growth factor CCell cultureEndothelium VascularTumor Suppressor Protein p53

description

Tumors of endothelial origin develop rarely. Until now, only two angiosarcoma (AS)-derived endothelial cell lines have been be isolated, ISO-HAS and AS-M. Both AS-derived endothelial cell lines presented the typical endothelial characteristics, such as the expression of CD31 and von Willebrand factor, but differed from normal endothelial cells in a nuclear expression of p53, in a delayed angiogenic reaction, and a reduced expression of caveolin. In addition, differences in the expression of cytokines and cell adhesion molecules responsive to proinflammatory stimuli were observed. While AS-M showed an expression pattern similar to that of human umbilical vein endothelial cells (HUVEC), ISO-HAS clearly differed from primary endothelial cells by a constitutive expression of E-selection, granulocyte macrophage colony-stimulating factor, and vascular endothelial cell adhesion molecule-1. Even though the telomeres of both AS-derived established cell lines were longer than telomeres of freshly isolated HUVEC, neither transcripts encoding telomerase nor telomerase activity were detected, suggesting that the tumor cells of endothelial origin may use a telomerase-independent mechanism for maintaining the telomere length. This observation has implications for development of therapeutic approaches for angiosarcoma.

10.1016/s0014-4800(03)00074-1https://pubmed.ncbi.nlm.nih.gov/14516778