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Growth hormone induces eNOS expression and nitric oxide release in a cultured human endothelial cell line
Author(s) -
Thum Thomas,
Tsikas Dimitris,
Frölich Jürgen C,
Borlak Jürgen
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)01356-5
Subject(s) - enos , medicine , endocrinology , nitric oxide , endothelial stem cell , nitric oxide synthase type iii , cell culture , intracellular , biology , hormone , chemistry , nitric oxide synthase , microbiology and biotechnology , biochemistry , in vitro , genetics
Growth hormone deficiency is linked to cardiovascular disease and particularly increased peripheral vascular resistance. Surprisingly, its role in endothelial nitric oxide (NO) synthetase (eNOS) regulation and NO release is basically unknown. We therefore studied the effects of different doses of somatotropin in cultures of a human endothelial cell line (EAhy926). We investigated expression and activity of eNOS, as well as other target genes known to be deregulated in cardiovascular disease including E‐selectin and the lectin‐like oxidized low density lipoprotein receptor. Treatment of cultured human endothelial cells with somatotropin resulted in significant ( P <0.05) increases of eNOS gene and protein expression, as well as NO release, whereas production of intracellular reactive oxygen species was significantly reduced, at the highest somatotropin dose level. The enhanced eNOS gene/protein expression and enzyme activity correlate well. Our findings are suggestive for a novel role of growth hormone in endothelial biology, and particularly NO production.