Selenium promotes proliferation of chondrogenic cell ATDC5 by increment of intracellular ATP content under serum deprivation.
Selenium (Se) is an essential micronutrient, and low Se intake in Se-deficient areas plays roles in an endemic osteochondropathy characterized by chondronecrosis in growth plate and articular cartilage. However, the biological activities of Se on cartilage are largely unknown. In this study, we examined the effects of Se on chondrogenic cell ATDC5 and the possible mechanisms involved. We demonstrated that Se stimulated ATDC5 cell proliferation under serum deprivation but not routine culture. Furthermore, Se promoted G1-phase cell cycle progression along with induction of cyclin D1 expression at the mRNA and protein level. Moreover, Se increased intracellular ATP content and decreased intracellular superoxide anion concentration without affecting intracellular redox status as estimated by ratio of the reduced and oxidized glutathione. In addition, suppression of intracellular ATP synthesis by glycolysis inhibitor or mitochondrial uncoupler both abrogated Se-mediated cyclin D1 induction. These findings suggest Se stimulates proliferation of chondrogenic cell ATDC5 through acceleration of cell cycle progression accompanied with cyclin D1 induction by enhancement of intracellular ATP content. This novel finding provides evidence for a role of Se in cartilage formation and degenerative processes and further supports the relationship between Se status and cartilage function that may lead to better utilization of Se for cartilage homeostasis.
Department of Genetics and Molecular Biology, Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi, China.
Jidong
J
Yan
Juan
J
Tian
Yuewen
Y
Zheng
Yan
Y
Han
Shemin
S
Lu
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D015153:Blotting, Western; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects*; D019902:Chondrocytes / Q000166:cytology / Q000378:metabolism*; D016895:Culture Media, Serum-Free / Q000494:pharmacology*; D019938:Cyclin D1 / Q000235:genetics / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D016193:G1 Phase / Q000187:drug effects; D019803:Glutathione Disulfide / Q000378:metabolism; D051379:Mice; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012643:Selenium / Q000494:pharmacology*; D013481:Superoxides / Q000378:metabolism; D013997:Time Factors
D016895:Culture Media, Serum-Free; D013481:Superoxides; D019938:Cyclin D1; D000255:Adenosine Triphosphate; D012643:Selenium; D019803:Glutathione Disulfide