Igf2 deletion alters mouse placenta endocrine capacity in a sexually dimorphic manner

内分泌学 生物 胎盘 性二态性 胎儿 内分泌系统 激素 细胞生物学 怀孕 遗传学
作者
Bethany R. L. Aykroyd,Simon J. Tunster,Amanda N. Sferruzzi‐Perri
出处
期刊:Journal of Endocrinology [Bioscientifica]
卷期号:246 (1): 93-108 被引量:31
标识
DOI:10.1530/joe-20-0128
摘要

The placenta regulates materno-fetal nutrient transfer and secretes hormones that enable maternal physiological support of the pregnancy. In mice, these functions are performed by the labyrinth (Lz) and junctional (Jz) zones, respectively. Insulin-like growth factor 2 (Igf2) is an imprinted gene expressed by the conceptus that is important for promoting fetal growth and placenta formation. However, the specific role of Igf2 in the Jz in regulating placental endocrine function and fetal development is unknown. This study used a novel model to investigate the effect of conditional loss of Igf2 in the Jz (Jz-Igf2UE) on placental endocrine cell formation and the expression of hormones and IGF signaling components in placentas from female and male fetuses. Jz-Igf2UE altered gross placental structure and expression of key endocrine and signaling genes in a sexually dimorphic manner. The volumes of spongiotrophoblast and glycogen trophoblast in the Jz were decreased in placentas from female but not male fetuses. Expression of insulin receptor was increased and expression the MAPK pathway genes (Mek1, P38α) decreased in the placental Jz of female but not male fetuses. In contrast, expression of the type-1 and -2 IGF receptors and the MAPK pathway genes (H-ras, N-ras, K-ras) was decreased in the placental Jz from male but not female fetuses. Expression of the steroidogenic gene, Cyp17a1, was increased and placental lactogen-2 was decreased in the placenta of both sexes. In summary, we report that Jz-Igf2UE alters the cellular composition, IGF signaling components and hormone expression of the placental Jz in a manner largely dependent on fetal sex.

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
一个小柠檬完成签到,获得积分10
刚刚
1秒前
英俊的铭应助zzy17779140061采纳,获得10
2秒前
可一发布了新的文献求助10
2秒前
充电宝应助Gangsta采纳,获得10
3秒前
Follow给Follow的求助进行了留言
4秒前
4秒前
kkm完成签到,获得积分10
5秒前
8秒前
踏雪飞鸿发布了新的文献求助10
8秒前
ohh发布了新的文献求助10
9秒前
LX完成签到 ,获得积分10
11秒前
ww完成签到,获得积分10
11秒前
12秒前
13秒前
oceanao应助博文采纳,获得10
13秒前
迷人的冰蓝完成签到,获得积分10
14秒前
14秒前
深情安青应助迅速枕头采纳,获得10
15秒前
Simlove发布了新的文献求助10
18秒前
Sherry完成签到,获得积分10
19秒前
吹吹晚风完成签到,获得积分10
20秒前
22秒前
科研通AI2S应助777777777采纳,获得10
22秒前
23秒前
牛逼man完成签到,获得积分10
23秒前
科目三应助科研通管家采纳,获得10
24秒前
小蘑菇应助科研通管家采纳,获得10
24秒前
Jasper应助科研通管家采纳,获得10
24秒前
桐桐应助科研通管家采纳,获得10
24秒前
李爱国应助科研通管家采纳,获得10
24秒前
研友_VZG7GZ应助科研通管家采纳,获得10
24秒前
搜集达人应助科研通管家采纳,获得10
24秒前
NexusExplorer应助科研通管家采纳,获得10
24秒前
24秒前
666完成签到,获得积分10
25秒前
26秒前
666发布了新的文献求助30
26秒前
27秒前
nini发布了新的文献求助10
28秒前
高分求助中
Spray / Wall-interaction Modelling by Dimensionless Data Analysis 2000
ALA生合成不全マウスでの糖代謝異常の分子機構解析 520
安全防范技术与工程 500
Mathematics and Finite Element Discretizations of Incompressible Navier—Stokes Flows 500
A real-time energy management strategy based on fuzzy control and ECMS for PHEVs 400
2024 Medicinal Chemistry Reviews 400
Актуализированная стратиграфическая схема триасовых отложений Прикаспийского региона. Объяснительная записка 360
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3191675
求助须知:如何正确求助?哪些是违规求助? 2841005
关于积分的说明 8030939
捐赠科研通 2504476
什么是DOI,文献DOI怎么找? 1337672
科研通“疑难数据库(出版商)”最低求助积分说明 638193
邀请新用户注册赠送积分活动 606684