| First Author | Tobita T | Year | 2019 |
| Journal | J Reprod Dev | Volume | 65 |
| Issue | 3 | Pages | 239-244 |
| PubMed ID | 30745494 | Mgi Jnum | J:277364 |
| Mgi Id | MGI:6315900 | Doi | 10.1262/jrd.2018-157 |
| Citation | Tobita T, et al. (2019) Lvrn expression is not critical for mouse placentation. J Reprod Dev 65(3):239-244 |
| abstractText | Preeclampsia is a systemic disease caused by abnormal placentation that affects both mother and fetus. It was reported that Laeverin (LVRN, also known as Aminopeptidase Q) was up-regulated in the placenta of preeclamptic patients. However, physiological and pathological functions of LVRN remained to be unknown. Here we characterized Lvrn function during placentation in mice. RT-PCR showed that Lvrn is expressed in both fetus and placenta during embryogenesis, and several adult tissues. When we overexpressed Lvrn in a placenta-specific manner using lentiviral vectors, we did not see any defects in both placentae and fetuses. The mice carrying Lvrn overexpressing placentas did not show any preeclampsia-like symptoms such as maternal high blood pressure and fetal growth restriction. We next ablated Lvrn by CRISPR/Cas9-mediated genome editing to see physiological function. In Lvrn ablated mice, maternal blood pressure during pregnancy was not affected, and both placentas and fetuses grew normally. Collectively, these results suggest that, LVRN is irrelevant to preeclampsia and dispensable for normal placentation and embryonic development in mice. |
