Effects of androgen on the folic acid‐induced inhibitions of endothelial cell proliferation and migration

Abstract

Folic acid (FA) has been suggested as an important daily dietary supplement, especially for women during pregnancy need to add a lot of FA to prevent some of the embryonic development of the lesions. Our previous studies have indicated that FA has anti‐angiogenic effect. However, there is no relevant studies indicated that pregnant women ingestion of FA induce lesions due to anti‐angiogenesis. Therefore, we proposed that estrogen might be able to antagonize the folic acid‐induced anti‐angiogenesis activity, and this hypothesis has been proved. However, previous studies showed endothelial cells also express androgen receptors (AR). Accordingly, this study was aimed to investigate whether androgen could influence the FA‐induced anti‐angiogenesis. We conducted in vitro study to investigate whether androgen has any impact on proliferation and migration. The preliminarydata showed that treatment with androgen agonist, R1881 or FA alone could inhibit cell proliferation and migration. However, co‐treatment will abolish the FA‐induced inhibitions on cell proliferation and migration. Moreover, we previously found that FA inhibits proliferation by increasing the levels of p21 and p27 proteins, and reduced the cell migration activity by inhibiting the RhoA activity. Thus, we examined the androgen on the signaling pathway involved in cell proliferation and migration. Our results showed R1881 could reduce the cSrc and up‐regulations of p21 and p27. Taken together, the results of this study suggest that activation of AR could abolish the FA‐induced inhibitions on endothelial cell proliferation and migration.