Background and ObjectivesThe thioredoxin (TRx) system is a ubiquitous thiol oxidoreductase pathway that regulates cellular reduction/oxidation status. Although endothelial cell (EC) hypoxic damage is one of the important pathophysiologic mechanisms of ischemic heart disease, its relationship to the temporal expression pattern of the TRx system has not yet been elucidated well. The work presented here was performed to define the expression pattern of the TRx system and its correlation with cellular apoptosis in EC lines in hypoxic stress. These results should provide basic clues for applying aspects of the TRx system as a therapeutic molecule in cardiovascular diseases.Subjects and MethodsHypoxia was induced with 1% O2, generated in a BBL GasPak Pouch (Becton Dickinson, Franklin Lakes, NJ, USA) in human endothelial progenitor cells (hEPC) and human umbilical vein endothelial cells (HUVEC). Apoptosis of these cells was confirmed by Annexin-V: Phycoerythrin flow cytometry. Expression patterns of TRx; TRx reductase; TRx interacting protein; and survival signals, such as Bcl-2 and Bax, in ECs under hypoxia were checked.ResultsApoptosis was evident after hypoxia in the two cell types. Higher TRx expression was observed at 12 hours after hypoxia in hEPCs and 12, 36, 72 hours of hypoxia in HUVECs. The expression patterns of the TRx system components showed correlation with EC apoptosis and cell survival markers.ConclusionHypoxia induced significant apoptosis and its related active changes of the TRx system were evident in human EC lines. If the cellular impact of TRx expression pattern in various cardiovascular tissues under hypoxia or oxidative stress was studied meticulously, the TRx system could be applied as a new therapeutic target in cardiovascular diseases, such as ischemic heart disease or atherosclerosis.
Background and Objectives:The degree of neointima formation after infliction of a carotid artery balloon injury in rats varies greatly depending on the sex, age, species and operational method. Strong variation is common, even within only a single control. This study attempted to find if there was any significant difference in neointima formation following a carotid artery balloon injury in 6 to 12 week old rats; the age commonly used in these types of experiments. Materials and Methods:A balloon injury was inflicted on the carotid arteries of male SpragueDawley rats at 6 (n=9, 250-270 g), 8 (n=8, 280-300 g) and 11 weeks (n=10, 320-340 g) of age. Two weeks postoperation, a histomorphometric analysis was carried out. The vascular smooth muscle cell proliferation was measured in situ via BrdU incorporation 2 days after injury infliction. Results:The neointima areas of the 6 week (0.22±0.04 mm
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