当前位置：
X-MOL 学术
›
Mol. Reprod. Dev.
›
论文详情
Our official English website, www.x-mol.net, welcomes your
feedback! (Note: you will need to create a separate account there.)
Fecundity is impaired in a mouse model of osteogenesis imperfecta.
Molecular Reproduction and Development ( IF 2.7 ) Pub Date : 2020-08-31 , DOI: 10.1002/mrd.23416 Arin K Oestreich 1 , Jenna A DeCata 1 , Janae D Akers 1 , Charlotte L Phillips 2 , Laura C Schulz 1
Molecular Reproduction and Development ( IF 2.7 ) Pub Date : 2020-08-31 , DOI: 10.1002/mrd.23416 Arin K Oestreich 1 , Jenna A DeCata 1 , Janae D Akers 1 , Charlotte L Phillips 2 , Laura C Schulz 1
Affiliation
|
Osteogenesis imperfecta (OI), or brittle bone disease, is most often caused by mutations in genes encoding type I collagen or proteins that process it. Women with OI have a small, but significant increase in risk of serious pregnancy complications including uterine rupture. Here, the OI mouse, Col1a2oim/oim, was used to examine the effects of collagen mutation on establishment and maintenance of pregnancy. Picrosirius birefringence was faint in Col1a2oim/oim uteri, indicating diminished collagen in the myometrium and endometrium. There was some evidence of increased uterine gland number (p = .055) and size (p = .12) in (p = .055) virgin uteri, though the they were not significantly different than controls. There were no differences in the number of corpora lutea, or the time from pairing to delivery of pups between Col1a2oim/oim and control dams, suggesting that ovulation and conception occur normally. However, when examined at Gestation Day 6.5 (postimplantation), gestation Day 10.5 (midpregnancy), and Postnatal Days 1–2, Col1a2oim/oim dams had significantly fewer viable pups than controls overall. In pairwise comparisons, the loss was only significant in the postnatal group, suggesting the gradual loss of pups over time. Overall, the Col1a2oim/oim mouse data suggest that OI impairs uterine function in pregnancy in a way that affects a small but significant number of fetuses.
中文翻译：
在成骨不全症小鼠模型中，生殖力受损。
成骨不全症（OI）或脆性骨病通常是由编码I型胶原蛋白或加工该蛋白的蛋白质的突变引起的。患有OI的妇女发生严重妊娠并发症（包括子宫破裂）的风险很小，但显着增加。在这里，OI小鼠Col1a2 oim / oim用于检查胶原蛋白突变对妊娠建立和维持的影响。Picrosirius双折射在Col1a2 oim / oim子宫中微弱，表明子宫内膜和子宫内膜中的胶原蛋白减少。有增大的子宫腺数（一些证据p = 0.055）和大小（p 中（= 0.12）p = 0.055）处女子宫，尽管它们与对照组没有显着差异。在Col1a2 oim / oim和对照大坝之间，黄体数量或从配对到成年幼崽的时间没有差异，表明排卵和受孕是正常的。但是，当在妊娠第6.5天（植入后），妊娠第10.5天（妊娠中期）和产后第1-2天进行检查时，Col1a2 oim / oim水坝的活仔数明显低于对照组。在成对比较中，这种损失仅在产后组中是显着的，这表明随着时间的流逝，幼崽逐渐消失。总体而言，Col1a2 oim / oim 小鼠数据表明，OI会以影响少量但大量胎儿的方式损害妊娠中的子宫功能。
更新日期：2020-10-07
中文翻译：
在成骨不全症小鼠模型中，生殖力受损。
成骨不全症（OI）或脆性骨病通常是由编码I型胶原蛋白或加工该蛋白的蛋白质的突变引起的。患有OI的妇女发生严重妊娠并发症（包括子宫破裂）的风险很小，但显着增加。在这里，OI小鼠Col1a2 oim / oim用于检查胶原蛋白突变对妊娠建立和维持的影响。Picrosirius双折射在Col1a2 oim / oim子宫中微弱，表明子宫内膜和子宫内膜中的胶原蛋白减少。有增大的子宫腺数（一些证据p = 0.055）和大小（p 中（= 0.12）p = 0.055）处女子宫，尽管它们与对照组没有显着差异。在Col1a2 oim / oim和对照大坝之间，黄体数量或从配对到成年幼崽的时间没有差异，表明排卵和受孕是正常的。但是，当在妊娠第6.5天（植入后），妊娠第10.5天（妊娠中期）和产后第1-2天进行检查时，Col1a2 oim / oim水坝的活仔数明显低于对照组。在成对比较中，这种损失仅在产后组中是显着的，这表明随着时间的流逝，幼崽逐渐消失。总体而言，Col1a2 oim / oim 小鼠数据表明，OI会以影响少量但大量胎儿的方式损害妊娠中的子宫功能。
京公网安备 11010802027423号