Elevation of adipsin, a complement activating factor, in the mouse placenta during spontaneous abortion.
The complement system is thought to be precisely regulated during pregnancy. We have examined specific gene profiles in mouse placentas causing spontaneous abortion and found notable up-regulation of adipsin, a complement activating factor. The aim of the present study was to determine the basic kinetics and localization of adipsin in the placenta and the difference in complement activity between normal placentas and placentas of abortuses. Normal and spontaneously absorbed implantation sites obtained from naturally-mated mouse uteri on days 10.5 and 14.5 of pregnancy were processed for histologic studies and protein purification. Adipsin immunoreaction was detected at the decidua basalis in normal placentas and additionally at the placental labyrinth in the absorbed placentas. The quantity of adipsin was increased in the absorbed placentas compared with the normal placentas. In concert with the increase in adipsin, the amounts of complement component 3 and degradation products were elevated and complemental activity was up-regulated in the absorbed placenta. These findings suggest that local expression of adipsin has a reproductive effect at the feto-maternal interface and possibly plays a role in spontaneous abortion.
TAKESHITA
Ai
A
Laboratory of Laboratory Animal Science, Department of Integrated Structural Biosciences, Division of Veterinary Science, Graduate School of Life and Environmental Biosciences, Osaka Prefecture University, Osaka 598-8531, Japan.
KONDO
Tomohiro
T
OKADA
Toshiya
T
KUSAKABE
Ken Takeshi
KT
D000022:Abortion, Spontaneous / Q000378:metabolism*; D000818:Animals; D003167:Complement Activation / Q000502:physiology*; D003176:Complement C3 / Q000378:metabolism; D011416:Complement Factor D / Q000378:metabolism; D005260:Female; D007150:Immunohistochemistry; D051379:Mice; D008810:Mice, Inbred C57BL; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D014599:Uterus / Q000378:metabolism / Q000473:pathology
D003176:Complement C3; D011416:Complement Factor D; C493491:complement factor D, mouse