Abstract

PURPOSE: Exercise positively regulates several immune functions. Phagocytic capacity of macrophages also enhances by exercise. Previous study reported that enhancement of the phagocytic capacity of macrophage is regulated by exercise-induced hormones, such as catecholamine and glucocorticoids. TAM receptors, the consist of Tyro3, Axl and MerTK, are contributed to phagocytize an apoptotic cells via indirect-binding to phosphatidylserine. However, the effects of glucocorticoid stimulation on TAM receptors expression in macrophages remain unclear. Here we shown that the determine the effects of glucocorticoid stimulation on TAM receptors expression in mouse macrophages. METHODS: RAW264 cell and J774.1cells, mouse macrophage cell line were maintained with DMEM medium and RPMI1640 medium containing 10% FBS and antibiotics. Also, primary macrophages from mouse tissues were incubated 10%FBS/DMEM. These macrophages were treated with glucocorticoid among 24 hours. The mRNA expression of TAM receptors in glucocorticoid-treated macrophages was measured by RT real-time PCR. Also, protein expression of TAM receptors in macrophages was measured with western blot analysis. In addition, Gas6 (protein of bridges TAM receptor to the phosphatidylserine) concentration in culture medium in macrophages was measured by ELISA assay. RESULTS: Tyro3 and MerTK expression, but not Axl expression, were significantly enhance in glucocorticoid-treated macrophages compared with untreated macrophages. Especially, MerTK expression was remarkable increase by glucocorticoid treatment. In contrast, significantly enhancement of Gas6 expression was no observed. CONCLUSIONS: Thus, the remarkable increased expression of MerTK had observed in mouse macrophage. Although increased expression of Tyro3 was also observed, its changes were not so much Tyro3 as MerTK. These results suggested that exercise-induced enhancement of phagocytic capacity in macrophages may relate to enhance the TAM receptors expression, especially MerTK.

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