The decline of pregnancy rate and abnormal uterine responsiveness of steroid hormones in aging mice

Li, Mengqi; Yao, Mengfei; Yan, Jiaqi; Li, Zilong; Gu, Xu; Lin, Shuai; Hu, Wei; Yang, Zeng‐Ming

doi:10.1016/j.repbio.2017.09.001

Cited by 16 publications

(14 citation statements)

References 37 publications

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“…Mice with deletion of Pgr or Stat3 in the uterus are infertile as their progesterone resistance leads to complete failure of decidualization ( 135 , 139 ). In recent studies into placental development with advanced maternal age in mice, it was shown that PGR and pSTAT3 levels are reduced in the uterine stroma of aged females, thus decreasing the ability of the endometrium to respond to progesterone ( 140 , 141 ). This causes a blunted and delayed decidualization response with reduced proliferation and differentiation of uterine stromal cells, thus retarding the development of the decidua by up to 2 days in aged pregnancies.…”

Section: Endometrial Causes Of Iugrmentioning

confidence: 99%

Regulation of Placental Development and Its Impact on Fetal Growth—New Insights From Mouse Models

2018

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The placenta is the chief regulator of nutrient supply to the growing embryo during gestation. As such, adequate placental function is instrumental for developmental progression throughout intrauterine development. One of the most common complications during pregnancy is insufficient growth of the fetus, a problem termed intrauterine growth restriction (IUGR) that is most frequently rooted in a malfunctional placenta. Together with conventional gene targeting approaches, recent advances in screening mouse mutants for placental defects, combined with the ability to rapidly induce mutations in vitro and in vivo by CRISPR-Cas9 technology, has provided new insights into the contribution of the genome to normal placental development. Most importantly, these data have demonstrated that far more genes are required for normal placentation than previously appreciated. Here, we provide a summary of common types of placental defects in established mouse mutants, which will help us gain a better understanding of the genes impacting on human placentation. Based on a recent mouse mutant screen, we then provide examples on how these data can be mined to identify novel molecular hubs that may be critical for placental development. Given the close association between placental defects and abnormal cardiovascular and brain development, these functional nodes may also shed light onto the etiology of birth defects that co-occur with placental malformations. Taken together, recent insights into the regulation of mouse placental development have opened up new avenues for research that will promote the study of human pregnancy conditions, notably those based on defects in placentation that underlie the most common pregnancy pathologies such as IUGR and pre-eclampsia.

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Section: Endometrial Causes Of Iugrmentioning

confidence: 99%

Regulation of Placental Development and Its Impact on Fetal Growth—New Insights From Mouse Models

2018

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“…A previous study demonstrated that estrogen levels are also upregulated in Rbpj d/d female mice, leading to abnormal decidualization and embryonic lethality [30]. In aged mice, the estrogen-responsive genes are downregulated [10,14]. The decrease of uterine estrogen response may contribute to the decline of pregnancy rate [14].…”

Section: Discussionmentioning

confidence: 97%

“…In aged mice, the estrogen-responsive genes are downregulated [10,14]. The decrease of uterine estrogen response may contribute to the decline of pregnancy rate [14]. It is possible that the increase of both estrogen and uterine estrogen response may result in the decline of pregnancy in the F3 group.…”

Section: Discussionmentioning

confidence: 99%

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Female Reproductive Failures in Mouse Adolescent Pregnancy

Yang¹,

Y²,

Pan³

et al. 2021

Preprint

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Background: There are around 300 million adolescent pregnancies worldwide, accounting for 11% of all births worldwide. Accumulating evidence demonstrates that many adverse perinatal outcomes are associated with adolescent pregnancies. However, how and why these abnormalities occur remain to be defined. Methods: To compare uterine maturity, implantation, decidualization and placental development between 25-30 days old and 3 months old mature female CD-1 strain mice. Both in vivo mouse pregnancy and in vitro cell culture were used. Western blot, real time RT-PCR, immunostaining and immunofluorescence were used to study the progress of pregnancy during two groups.Results: We found the litter size of adolescent pregnancy is significantly decreased from F1 to F3 generations compared to mature pregnancy. On days 8 and 12 of pregnancy, multiple abnormalities in placental and decidual developments appear in F3 adolescent pregnancy. On days 5 and 8, uterine endoplasmic reticulum stress is dysregulated compared to mature pregnancy. Embryo implantation and decidualization are also compromised in adolescent pregnancy. Many genes are abnormally expressed in adolescent estrous uteri. Conclusion: The uterine immaturities and abnormal implantation may cause multiple pregnancy failures in adolescent pregnancy.

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“…Male ICR mice (2 months old and 14 months old) were purchased from CLEA Japan Inc Several criteria show that 14‐month‐old mice correspond to senescent staged mouse 30,31 . All procedures and protocols are approved by the committee for animal researches at Wakayama Medical University, Wakayama, Japan (approval number: 867).…”

Section: Methodsmentioning

confidence: 99%

3D reconstruction and histopathological analyses on murine corporal body

Hashimoto

Kajimoto

Ueda

et al. 2021

Reprod Medicine & Biology

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Purpose Erectile dysfunction (ED) is one of the increasing diseases with aging society. The basis of ED derived from local penile abnormality is poorly understood because of the complex three‐dimensional (3D) distribution of sinusoids in corpus cavernosum (CC). Understanding the 3D histological structure of penis is thus necessary. Analyses on the status of regulatory signals for such abnormality are also performed. Methods To analyze the 3D structure of sinusoid, 3D reconstruction from serial sections of murine CC were performed. Histological analyses between young (2 months old) and aged (14 months old) CC were performed. As for chondrogenic signaling status of aged CC, SOX9 and RBPJK staining was examined. Results Sinusoids prominently developed in the outer regions of CC adjacent to tunica albuginea. Aged CC samples contained ectopic chondrocytes in such regions. Associating with the appearance of chondrocytes, the expression of SOX9, chondrogenic regulator, was upregulated. The expression of RBPJK, one of the Notch signal regulators, was downregulated in the aged CC. Conclusions Prominent sinusoids distribute in the outer region of CC which may possess important roles for erection. A possibility of ectopic chondrogenesis induced by alteration of SOX9/Notch signaling with aging is indicated.

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The decline of pregnancy rate and abnormal uterine responsiveness of steroid hormones in aging mice

Cited by 16 publications

References 37 publications

Regulation of Placental Development and Its Impact on Fetal Growth—New Insights From Mouse Models

Regulation of Placental Development and Its Impact on Fetal Growth—New Insights From Mouse Models

Female Reproductive Failures in Mouse Adolescent Pregnancy

3D reconstruction and histopathological analyses on murine corporal body

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