title: Effects of selenium deficiency on expression of selenoproteins in bovine arterial endothelial cells.
abstract: Damage to the vascular endothelium by reactive oxygen species causes many cardiovascular diseases including atherosclerosis. Such damage can be prevented by selenium (Se), which is thought to exert its actions mainly through the expression of selenoproteins. Se deficiency increased the susceptibility to tert-butylhydroperoxide (t-BuOOH) and enhanced lipid peroxidation in bovine arterial endothelial cells (BAEC). We investigated the effects of Se deficiency on the expression of the selenoproteins in BAEC. 75Se metabolic labeling analysis and RT-PCR analysis revealed that BAEC expressed two glutathione peroxidase (GPx) isozymes, cytosolic GPx (cGPx) and phospholipid hydroperoxide GPx (PHGPx), three thioredoxin reductase (TrxR) isozymes, TrxR1, TrxR2 and TrxR3, and selenoprotein P (SelP). Se deficiency reduced both enzyme activity and mRNA level of cGPx, but did not affect those of PHGPx. SelP mRNA level was also reduced by Se deficiency, although the extent of reduction was much smaller than that of cGPx mRNA. We further found that TrxR activity was also decreased by Se deficiency but none of the mRNA levels of TrxR isozymes were reduced. These results indicate that vascular endothelial cells express several selenoproteins including cGPx, PHGPx, TrxR isozymes and SelP which might play important roles in the defense system against oxidative stresses and that the expressions of these selenoproteins are differently regulated by Se status.
authors.affiliation: Department of Public Health and Molecular Toxicology, School of Pharmaceutical Sciences, Kitasato University, Tokyo, Japan. haras@pharm.kitasato
authors.forename: S
authors.initials: S
authors.lastname: Hara
authors.forename: Y
authors.initials: Y
authors.lastname: Shoji
authors.forename: A
authors.initials: A
authors.lastname: Sakurai
authors.forename: K
authors.initials: K
authors.lastname: Yuasa
authors.forename: S
authors.initials: S
authors.lastname: Himeno
authors.forename: N
authors.initials: N
authors.lastname: Imura
mesh_terms: D000818:Animals; D001158:Arteries / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D015152:Blotting, Northern; D002417:Cattle; D002478:Cells, Cultured; D015237:Dinoprost / Q000031:analogs & derivatives*; D004591:Electrophoresis, Polyacrylamide Gel; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D028441:F2-Isoprostanes / Q000096:biosynthesis; D014176:Protein Biosynthesis; D011506:Proteins; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012643:Selenium / Q000172:deficiency*; D012644:Selenium Radioisotopes; D051149:Selenoprotein P; D051140:Selenoproteins; D013880:Thioredoxin-Disulfide Reductase / Q000378:metabolism
chemical_list: D028441:F2-Isoprostanes; D011506:Proteins; D012333:RNA, Messenger; D012644:Selenium Radioisotopes; D051149:Selenoprotein P; D051140:Selenoproteins; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost; D013880:Thioredoxin-Disulfide Reductase; D012643:Selenium