Prevention of intrauterine fetal growth restriction by administrating C1q/TNF-related protein 6, a specific inhibitor of the alternative complement pathway.

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Abstrakt

Tytuł:: Prevention of intrauterine fetal growth restriction by administrating C1q/TNF-related protein 6, a specific inhibitor of the alternative complement pathway.
Autorzy:: Kurokawa M; Women's Lifecare Medicine, Obstetrics and Gynecology, School of Medicine, Osaka City University, 545-8585, Osaka, Japan.; Graduate School of Medicine, Reproductive Science, Osaka City University, Osaka, 545-8585, Japan.
Takeshita A; Graduate School of Medicine, Reproductive Science, Osaka City University, Osaka, 545-8585, Japan.; Department of Anatomy and Neurobiology, Faculty of Medicine, Kindai University, Osaka, 589-8511, Japan.
Hashimoto S; Graduate School of Medicine, Reproductive Science, Osaka City University, Osaka, 545-8585, Japan. .
Koyama M; Women's Lifecare Medicine, Obstetrics and Gynecology, School of Medicine, Osaka City University, 545-8585, Osaka, Japan.
Morimoto Y; HORAC Grand Front Osaka Clinic, Osaka, 530-0011, Japan.
Tachibana D; Women's Lifecare Medicine, Obstetrics and Gynecology, School of Medicine, Osaka City University, 545-8585, Osaka, Japan.
Źródło:: Journal of assisted reproduction and genetics [J Assist Reprod Genet] 2022 Sep; Vol. 39 (9), pp. 2191-2199. Date of Electronic Publication: 2022 Jul 30.
Typ publikacji:: Journal Article; Randomized Controlled Trial, Veterinary
Język:: English
Imprint Name(s):: Publication: <2004- >: Amsterdam : Springer
Original Publication: New York : Plenum Press, c1992-
MeSH Terms:: Abortion, Spontaneous*/metabolism
Abortion, Spontaneous*/prevention & control
Fetal Growth Retardation*/drug therapy
Adipokines/metabolism ; Animals ; Complement C1q/metabolism ; Complement Pathway, Alternative ; Female ; Male ; Mice ; Mice, Inbred CBA ; Mice, Inbred DBA ; Placenta/metabolism ; Pregnancy
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Grant Information:: 20K09674 the Japan Society for the Promotion of Science; 18H06257 the Japan Society for the Promotion of Science; 19K18649 the Japan Society for the Promotion of Science
Contributed Indexing:: Keywords: Abortion; Complement Alternative pathway; Recurrent pregnant failure; Spiral artery
Substance Nomenclature:: 0 (Adipokines)
0 (CTRP6 protein, mouse)
80295-33-6 (Complement C1q)
Entry Date(s):: Date Created: 20220730 Date Completed: 20220916 Latest Revision: 20230902
Update Code:: 20240104
PubMed Central ID:: PMC9474761
DOI:: 10.1007/s10815-022-02582-1
PMID:: 35907048
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Purpose: The latest treatments do not sufficiently prevent miscarriage and fetal growth restriction (FGR) in pregnant women. Here, we assessed the effects of a human protein, CTRP6, that specifically inhibits the activation of the alternative complement pathway on miscarriage, fetal and placental development.
Methods: Pregnant CBA/J mice mated with DBA/2 male mice as a model of spontaneous abortion and FGR were randomly divided into the control and CTRP6 groups. In the CTRP6 group, the mice were intravenously administered CTRP6 on days 4.5 and 6.5 post-conception (dpc). The abortion rate and fetal and placental weights on 14.5 dpc were examined. Remodeling of the spiral artery was also assessed.
Results: The abortion rate in the CTRP6 group (13%) was reduced compared to the control group (21%), but there was no statistical difference. The placental and fetal weights in the CTRP6 group were also heavier than those in the control (P < 0.05). Moreover, the thickness of the blood vessel wall in the CTRP6 group was significantly thinner than that in the control (P < 0.05) and comparable to that in the non-abortion model (CBA/J x BALB). The ratio of the inner-per-the-outer diameter of the spiral artery increased more in the CTRP6 group than that in the control (P < 0.05). As well, the Th1/Th2 cytokine ratio was significantly reduced by CTRP6 treatment.
Conclusions: Taken together, the supplementation with a protein that regulates the alternative complement pathway in vivo improves FGR and promotes spiral artery remodeling in a mouse model of miscarriage and FGR.
(© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

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