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. 2019 Jun 26;10:420. doi: 10.3389/fendo.2019.00420

Figure 3.

Figure 3

The pro-phagocytic effects of estrogen via ERβ require mobilization of annexin A1. (A) Treatment of primary microglia from wild-type mice with 17β-estradiol (100 nM, 16 h) promotes phagocytosis of apoptotic PC12 cells, whereas similar treatment of AnxA1−/− primary microglia causes a significant further inhibition in their phagocytic ability; data are means ± sem, n = 3, *p < 0.05 vs. untreated controls, +p < 0.05 vs. similarly treated wild-type group. (B) Treatment of BV2 cells for 16 h with 17β-estradiol or the ERβ agonist DPN, but not the GPER agonist G1, enhances production of AnxA1 mRNA; data are means ± sem, n = 3, *p < 0.05 vs. untreated controls. (C) Treatment of BV2 cells for 16 h with 17β-estradiol, DPN or G1 enhances total cellular AnxA1 content; data are means ± sem, n = 3, *p < 0.05 vs. untreated controls. (D) Treatment of BV2 cells for 16 h with DPN enhances, whilst similar treatment with G1 reduces, surface expression of AnxA1; data are means ± sem, n = 3, *p < 0.05 vs. untreated controls. (E) Treatment of BV2 cells for 16 h with 17β-estradiol or DPN but not G1 enhances release of AnxA1 into the culture medium; data are means ± sem, n = 3, *p < 0.05 vs. untreated controls.