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Adenosine stimulates mitochondrial biogenesis in microvascular endothelial cells
Author(s) -
Kalogeris Theodore J.,
Korthuis Ronald J.
Publication year - 2009
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.23.1_supplement.965.13
Subject(s) - mitochondrial biogenesis , adenosine , tfam , mitochondrion , microbiology and biotechnology , endothelial stem cell , biology , chemistry , endocrinology , biochemistry , in vitro
Modulation of mitochondrial biogenesis may contribute to the vasculo‐protective effects of preconditioning. We tested whether adenosine (Ado), a mediator of ethanol preconditioning in vivo, could influence mitochondrial biogenesis in human microvascular endothelial cells (HMEC‐1). Cells were treated daily with or without Ado (1 µM) for 1‐8 days. At each time point, whole‐cell protein was probed for expression of several markers and mediators of mitochondrial biogenesis. Compared with control cells, Ado elicited time‐dependent increases in PGC‐1α, NRF‐2, porin, and cytochrome c oxidase (COX‐IV, subunit II), but had no effect on expression of either GAPDH or β‐actin; PGC‐1α and NRF‐2 were significantly increased by 1.5‐2‐fold after 2 days of Ado treatment and peaked at levels 3‐4‐fold higher than control by day 5. Porin showed a biphasic response, peaking on days 2‐3 (3‐fold higher than control) and rising to levels 4‐5‐fold higher than control by day 8. COX‐IV was unresponsive until day 6; by day 8, COX‐IV expression was 3‐4‐fold higher than control. In other studies, cells treated with Ado for 8 days showed a significant (42%) increase in oxidation of MTT to MTT‐formazan compared with control cells. These results are consistent with an Ado‐triggered program of mitochondrial biogenesis in endothelial cells which may contribute to vasculo‐protective effects of preconditioning. Supported by AA14945.