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Inflammatory and angiogenic potential of primary and hTERT‐transduced human coronary artery endothelial cells
Author(s) -
Baumer Yvonne,
Ivanov Svetlana,
Schlosshauer Burkhard
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.644.3
Subject(s) - telomerase reverse transcriptase , matrigel , endothelial stem cell , microbiology and biotechnology , telomerase , cell culture , angiogenesis , downregulation and upregulation , endothelium , biology , chemistry , cancer research , immunology , in vitro , endocrinology , genetics , gene
In vascular research the use of endothelial cell (EC) lines would be desirable because of often high priced primary EC which display donor diversity. However, endothelial cell lines are often insufficiently characterized or represent irrelevant models because of cellular dedifferentiation like the reduced inflammatory response and permeability properties or deregulated protein expression. We established a human coronary artery EC line (HCAEC) by overexpression of human telomerase reverse transcriptase (hTERT). In comparative analyses we showed that primary and hTERT transduced HCAEC displayed comparable characteristics. These studies included: 1) detection of 9 endothelial and nonendothelial proteins by fluorescence‐microscopy (IF), western blot‐ and fluorescence activated cell sorting (FACS)‐analysis, 2) uptake of ac‐LDL by IF and FACS, 3) upregulation of ICAM‐1 after pro‐inflammatory stimulation, 4) analysis of changes in endothelial barrier function by measuring transendothelial electrical resistance and 5) detection of angiogenic properties by analyzing migration potential, Matrigel™ tube formation‐ and a fibroblast co‐culture‐assays. We conclude that hTERT overexpression did not alter typical endothelial characteristics. hTERT immortalized HCAEC are a valuable tool for endothelial research. Supported by the German Ministry of Education and Research (BMBF) # 01GU0727.