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Isolation of Mouse Endometrial Epithelial and Stromal Cells for In Vitro Decidualization
Published on: March 2, 2017
CXCL12 expression in aborted mouse uteri induced by IFN-γ: Potential anti-inflammatory effect involves in endometrial
Hu-He Chao1, Lin Li1, Xiao Gao1
1Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Chaoyang, Beijing 100026, China.
Anti-inflammation is a key process to restore tissue integrity and function. CXCL12 is a homeostasis chemokine, which plays a coordinating role in organogenesis, tumorigenesis and regeneration. In the present study we found that the uterus of abortion mice showed different histo-morphological changes with the development of abortion. The expression of chemokine CXCL12 and its receptor CXCR4 in abortion uterus showed a time-dependent pattern. Compared with normal pregnancy, the expression of CXCL12 and CXCR4 did not change in the uterus of GD7 abortion mice, but increased significantly in the uterus of GD8 and GD10 abortion mice. However, the expression of IFN-γ increased significantly in the uterus of GD7 abortion mice, while there was no significant change detected in GD8 aborted mice uterus. Our further data show that the expression of CXCL12 is not regulated by IFN-γ in endometrial stromal cell culture system in vitro. The treatment of CXCL12 significantly inhibits the expression of IFN-γ in in vitro cultured stromal cells and splenic monocytes. This suggests that CXCL12 may play an anti-inflammatory role in the uterus of abortion mice to promote the process of endometrial restoration after abortion, rather than participate in the process of abortion as a response molecule of IFN-γ.
Anti-inflammation is a key process to restore tissue integrity and function. CXCL12 is a homeostasis chemokine, which plays a coordinating role in organogenesis, tumorigenesis and regeneration. In the present study we found that the uterus of abortion mice showed different histo-morphological changes with the development of abortion. The expression of chemokine CXCL12 and its receptor CXCR4 in abortion uterus showed a time-dependent pattern. Compared with normal pregnancy, the expression of CXCL12 and CXCR4 did not change in the uterus of GD7 abortion mice, but increased significantly in the uterus of GD8 and GD10 abortion mice. However, the expression of IFN-γ increased significantly in the uterus of GD7 abortion mice, while there was no significant change detected in GD8 aborted mice uterus. Our further data show that the expression of CXCL12 is not regulated by IFN-γ in endometrial stromal cell culture system in vitro. The treatment of CXCL12 significantly inhibits the expression of IFN-γ in in vitro cultured stromal cells and splenic monocytes. This suggests that CXCL12 may play an anti-inflammatory role in the uterus of abortion mice to promote the process of endometrial restoration after abortion, rather than participate in the process of abortion as a response molecule of IFN-γ.
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