Selenium improves stem cell potency by stimulating the proliferation and active migration of 3T3-L1 preadipocytes

Abstract

Selenium is a trace nutrient element that protects cells against oxidative damage. In this study, the potential of selenium to improve stem cell potency through active proliferation and migration of 3T3-L1 preadipocytes was investigated, together with the underlying molecular mechanisms. The results indicated that selenium applied for 24 h stimulated cell proliferation up to 20% compared to untreated control cells. Selenium induced the expression of cyclin-dependent kinase (CDK) 1 and CDK2, which are known to regulate G2/M progression, and significantly downregulated the CDK inhibitors p21 and p27. Selenium also activated the expression of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, as well as extracellular signal-regulated kinase (ERK). Although LY294002, an inhibitor of PI3K, significantly inhibited the selenium-induced cell proliferation of the 3T3-L1 preadipocytes, PD98059, an inhibitor of ERK, did not affect selenium-induced active proliferation. These results clearly indicate that selenium stimulated cell proliferation through cell cycle progression and PI3K/Akt activation, but not through ERK activation. Furthermore, selenium increased 3T3-L1 cell migration, which was associated with the induction of matrix metalloproteinase (MMP)-2 and MMP-9. Taken together, the current findings suggest that selenium can stimulate stem cell potency by increasing the proliferation and active migration of 3T3-L1 cells.