Effects of selenium supplementation on expression of endothelin-1 and its receptors in pulmonary microvascular endothelial cells from chick embryos.
The objective of this study was to evaluate the effects of supplemental selenium (Se) on expression of endothelin-1 (ET-1) and its receptors in cultured chick embryos pulmonary microvascular endothelial cells (PMVECs). To accomplish this, PMVECs were treated in Se-deficient or Se-supplement (12, 24, 50, 100 ng/ml) culture medium for 48 h. Low Se medium was achieved by reducing serum concentrations and the essential growth factors were added. After the incubation, the effects of supplemental Se on ET-1 and its receptors gene expression were assessed by quantitative real-time PCR (qRT-PCR). Compared with the control group, our results showed that among the different concentrations of Se supplement, the levels of ET-1 gene expression treated with both the moderate Se doses (24, 50 ng/ml, P < 0.01, P < 0.01, respectively) and the high doses (100 ng/ml, P < 0.05) were noticeably decreased, the low-dose group (12 ng/ml), which showed no changes. Meanwhile, Se supplement (24, 50, 100 ng/ml) was found to be effective in reducing the expression levels of ETA (P < 0.01, P < 0.05, P < 0.05, respectively) in cultured PMVECs grown in low Se medium. However, there were no significant changes (P > 0.05) in ETB mRNA levels during the cell proliferation. These observations indicated that Se may play both direct and indirect role in the regulation of ET-1 and its receptors gene expression and their production in avian PMVECs. Se supplement decreases in ET-1 and ETA production in Se-deficient PMVECs may partly explain the mechanism of the protective effects of the Se on the cardiovascular system.
College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, People's Republic of China.
Jianfeng
J
Gao
Ding
D
Zhang
Kerong
K
Zhang
Mengyuan
M
Liu
Zhaoqing
Z
Han
Jiakui
J
Li
D000818:Animals; D030161:Avian Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000517:prevention & control; D002470:Cell Survival; D002478:Cells, Cultured; D002642:Chick Embryo; D015536:Down-Regulation; D065130:Endothelin A Receptor Antagonists; D019332:Endothelin-1 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000166:cytology / Q000196:embryology / Q000378:metabolism*; D018507:Gene Expression Regulation, Developmental; D008168:Lung / Q000166:cytology / Q000196:embryology / Q000378:metabolism*; D055806:Microvessels / Q000166:cytology / Q000196:embryology / Q000378:metabolism*; D009994:Osmolar Concentration; D020011:Protective Agents / Q000378:metabolism / Q000627:therapeutic use; D012333:RNA, Messenger / Q000378:metabolism; D044022:Receptor, Endothelin A / Q000235:genetics / Q000378:metabolism*; D044023:Receptor, Endothelin B / Q000235:genetics / Q000378:metabolism; D015203:Reproducibility of Results; D012643:Selenium / Q000172:deficiency / Q000378:metabolism* / Q000627:therapeutic use; D018038:Sodium Selenite / Q000378:metabolism
D030161:Avian Proteins; D065130:Endothelin A Receptor Antagonists; D019332:Endothelin-1; D020011:Protective Agents; D012333:RNA, Messenger; D044022:Receptor, Endothelin A; D044023:Receptor, Endothelin B; D012643:Selenium; D018038:Sodium Selenite