G-CSF: One of The Vehicles for Communication Between Trophoblasts and Macrophages, Which May Cause Problems in Recurrent Spontaneous Abortion
Peng Gao, Haiyi Liu, Ying Zha, Lijie Wei, Xuan Zhou, Shenglan Zhu, Huiting Zhang, Xuan Gao, Yi Jiang, YuTing Chen, Jiaqi Li, Jingyi Zhang (+3 others)
The etiology of about half of the patients with recurrent spontaneous abortion (RSA) remains unclear, and the imbalance of the immune inflammatory response at the mother-foetal interface may be one of the keys to the onset. Granulocyte-colony stimulating factor (G-CSF) is thought to have a protective effect on pregnancy, and its absence may lead to pregnancy failure, but the evidence is scant. This study aims at investigating whether the loss of G-CSF induced RSA by affecting cell communication at the maternal-foetal interface.
G-CSF was mainly expressed in villus rather than decidua, and the expression in RSA tissues was lower than that in normal tissues. Down-regulation of G-CSF in trophoblasts resulted in decreased cell activity. Trophoblast-derived exosomes inhibited macrophage activation, while G-CSF free exosomes did not. Intraperitoneal injection of G-CSF improved the pregnancy outcome of RSA mice, and the expression of G-CSF and its receptor at the mother-foetal interface also changed.
The expression of G-CSF was found to be decreased in villi of patients with RSA. The absence of G-CSF weakens the immune suppression of trophoblasts against macrophages, and the function of trophoblasts is impaired, which may be a key factor in the occurrence of RSA. G-CSF decreased the rate of abortion in RSA mice, and might provide some assistance in the treatment of patients with RSA.
Archived Files and Locations
|application/pdf 774.2 kB ||
|application/pdf 782.6 kB ||
access all versions, variants, and formats of this works (eg, pre-prints)
Crossref Metadata (via API)