Elevation of adipsin, a complement activating factor, in the mouse placenta during spontaneous abortion

Area of Science:

• Reproductive immunology
• Complement system biology
• Maternal-fetal interface research

Background:

• The complement system is crucial for pregnancy, requiring precise regulation.
• Aberrant complement activation is implicated in pregnancy complications.
• Adipsin, a complement-activating factor, has been observed to be upregulated in placentas associated with spontaneous abortion.

Purpose of the Study:

• To investigate the kinetics and localization of adipsin in mouse placentas.
• To compare complement activity between normal and spontaneously aborted placentas.
• To elucidate the role of adipsin in spontaneous abortion.

Main Methods:

• Histological examination of normal and aborted mouse implantation sites (days 10.5 and 14.5).
• Immunohistochemical detection of adipsin.
• Protein purification and quantification of adipsin.
• Measurement of complement component 3 and degradation products.
• Assessment of complemental activity.

Main Results:

• Adipsin immunoreaction was found in the decidua basalis of normal placentas.
• Adipsin was also detected in the placental labyrinth of aborted placentas.
• Aborted placentas showed increased adipsin quantity compared to normal placentas.
• Elevated levels of complement component 3 and its degradation products were observed in aborted placentas.
• Overall complemental activity was up-regulated in aborted placentas.

Conclusions:

• Local adipsin expression influences reproductive outcomes at the feto-maternal interface.
• Adipsin may play a significant role in the pathogenesis of spontaneous abortion.
• Targeting adipsin or complement pathways could offer therapeutic strategies for recurrent pregnancy loss.