|  Help  |  About  |  Contact Us

Publication : Preeclampsia-Like Features and Partial Lactation Failure in Mice Lacking Cystathionine γ-Lyase-An Animal Model of Cystathioninuria.

First Author  Akahoshi N Year  2019
Journal  Int J Mol Sci Volume  20
Issue  14 PubMed ID  31319489
Mgi Jnum  J:290730 Mgi Id  MGI:6443405
Doi  10.3390/ijms20143507 Citation  Akahoshi N, et al. (2019) Preeclampsia-Like Features and Partial Lactation Failure in Mice Lacking Cystathionine gamma-Lyase-An Animal Model of Cystathioninuria. Int J Mol Sci 20(14):3507
abstractText  Elevated plasma homocysteine levels are considered as a risk factor for cardiovascular diseases as well as preeclampsia-a pregnancy disorder characterized by hypertension and proteinuria. We previously generated mice lacking cystathionine gamma-lyase (Cth) as cystathioninuria models and found them to be with cystathioninemia/homocysteinemia. We investigated whether Cth-deficient (Cth(-/-)) pregnant mice display any features of preeclampsia. Cth(-/-) females developed normally but showed mild hypertension (~10 mmHg systolic blood pressure elevation) in late pregnancy and mild proteinuria throughout development/pregnancy. Cth(-/-) dams had normal numbers of pups and exhibited normal maternal behavior except slightly lower breastfeeding activity. However, half of them could not raise their pups owing to defective lactation; they could produce/store the first milk in their mammary glands but not often provide milk to their pups after the first ejection. The serum oxytocin levels and oxytocin receptor expression in the mammary glands were comparable between wild-type and Cth(-/-) dams, but the contraction responses of mammary gland myoepithelial cells to oxytocin were significantly lower in Cth(-/-) dams. The contraction responses to oxytocin were lower in uteruses isolated from Cth(-/-) mice. Our results suggest that elevated homocysteine or other unknown factors in preeclampsia-like Cth(-/-) dams interfere with oxytocin that regulates milk ejection reflex.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

3 Bio Entities

Trail: Publication

0 Expression