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Pro‐atherogenic factors induce telomerase inactivation in endothelial cells through an Akt‐dependent mechanism
Author(s) -
Breitschopf Kristin,
Zeiher Andreas M,
Dimmeler Stefanie
Publication year - 2001
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(01)02272-4
Subject(s) - telomerase , protein kinase b , pi3k/akt/mtor pathway , angiogenesis , telomerase reverse transcriptase , microbiology and biotechnology , telomere , kinase , chemistry , mechanism (biology) , cancer research , biology , signal transduction , biochemistry , dna , gene , philosophy , epistemology
Advanced aging may contribute to impairment of angiogenesis and development of vascular diseases. Telomerase was shown to delay endothelial cell (EC) senescence. Therefore, we determined the regulation of telomerase activity in EC. Inhibition of phosphoinositol 3‐kinase (PI3K) suppressed telomerase activity, whereas inhibitors directed against ERK1/2 or protein kinase C had no effect. Dominant negative Akt significantly reduced telomerase activity. Moreover, pro‐atherogenic stimuli such as oxidized low density lipoprotein led to an inactivation of Akt and diminished telomerase activity. Thus, the PI3K/Akt pathway plays an important role in the regulation of telomerase activity. Pro‐atherosclerotic factors impair telomerase activity and thereby may promote EC aging.