Signaling mechanisms of gene-environment interactions in female reproductive

女性生殖基因-环境相互作用的信号机制

基本信息

  • 批准号:
    10594545
  • 负责人:
  • 金额:
    $ 20.25万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2022
  • 资助国家:
    美国
  • 起止时间:
    2022-04-01 至 2025-03-31
  • 项目状态:
    未结题

项目摘要

Project Summary/Abstract Congenital anomalies of the female reproductive tract (FRT) occur in approximately 5% of live birth in females. These conditions are congenital, but often go undetected until puberty when the patients fail to menstruate and suffer periodic lower abdominal pain; if left untreated, they lead to infertility and death during pregnancy or childbirth. The anomalies have complex clinical presentations with the etiology still poorly understood. Given that FRT anomaly has both familial and sporadic cases, the causative agents are likely to be complex, involving genes, environmental factors, or both. To date, the multifactorial etiology and the mechanisms of gene- environment interactions in congenital FRT anomalies are largely unexplored. We have recently identified Map3k1 loss-of-function as a novel genetic condition of congenital FRT anomaly - Map3k1 inactivation in mice is associated with developmental FRT defects and infertility in females. Map3k1 encodes a protein kinase, an upstream regulator of the MAPK pathways that crosstalk with diverse environmental signals and developmental pathways. We have shown that Map3k1 loss-of-function could aggravate the developmental toxicity of dioxin, a ubiquitous environmental pollutant. Moreover, dioxin is also a reproductive toxicant that induces FRT defects similar to those observed in the Map3k1-null mice. In the current proposal, we will test the hypothesis, supported by preliminary evidence, that Map3k1 mutation plus dioxin constitute the multifactorial etiology that converges on WNT inhibition to cause congenital FRT anomalies. We will use an in vivo genetic approach to examine whether Map3k1 mutation plus dioxin exposure potentiate the incidence and/or the severity of FRT defective phenotypes, whether the dioxin receptor, Ah receptor (AHR), mediates FRT toxicity, and whether the gene- environment interactions repress WNT activity. We will combine mouse genetics, molecular histopathogenesis, and laser capture microdissection coupled with global gene expression profiling to delineate the biological processes and molecular pathways affected by genetic and environmental insults in FRT development. We aim to understand the molecular details of how gene-environment interactions contribute to congenital female reproductive anomaly, with the long-term future goal of using this knowledge to prevent and treat this prevalent devastating disease affecting women’s health and reproductivity.
项目总结/文摘

项目成果

期刊论文数量(0)
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YING XIA其他文献

YING XIA的其他文献

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{{ truncateString('YING XIA', 18)}}的其他基金

Signaling mechanisms of gene-environment interactions in female reproductive
女性生殖基因-环境相互作用的信号机制
  • 批准号:
    10448935
  • 财政年份:
    2022
  • 资助金额:
    $ 20.25万
  • 项目类别:
Integrative Technologies Support Core
综合技术支持核心
  • 批准号:
    9903301
  • 财政年份:
    2020
  • 资助金额:
    $ 20.25万
  • 项目类别:
Gene-environment interactions in epithelial morphogenesis
上皮形态发生中的基因-环境相互作用
  • 批准号:
    10619541
  • 财政年份:
    2019
  • 资助金额:
    $ 20.25万
  • 项目类别:
Gene-environment interactions in epithelial morphogenesis
上皮形态发生中的基因-环境相互作用
  • 批准号:
    10382399
  • 财政年份:
    2019
  • 资助金额:
    $ 20.25万
  • 项目类别:
Gene-environment interactions in epithelial morphogenesis
上皮形态发生中的基因-环境相互作用
  • 批准号:
    9912166
  • 财政年份:
    2019
  • 资助金额:
    $ 20.25万
  • 项目类别:
Gene-Environment Interactions in Eyelid Morphogenesis
眼睑形态发生中的基因-环境相互作用
  • 批准号:
    8770085
  • 财政年份:
    2014
  • 资助金额:
    $ 20.25万
  • 项目类别:
A new strategy for protection from cerebral ischemia
预防脑缺血的新策略
  • 批准号:
    8217282
  • 财政年份:
    2009
  • 资助金额:
    $ 20.25万
  • 项目类别:
A new strategy for protection from cerebral ischemia
预防脑缺血的新策略
  • 批准号:
    7762239
  • 财政年份:
    2009
  • 资助金额:
    $ 20.25万
  • 项目类别:
A new strategy for protection from cerebral ischemia
预防脑缺血的新策略
  • 批准号:
    7581636
  • 财政年份:
    2009
  • 资助金额:
    $ 20.25万
  • 项目类别:
A new strategy for protection from cerebral ischemia
预防脑缺血的新策略
  • 批准号:
    8197611
  • 财政年份:
    2009
  • 资助金额:
    $ 20.25万
  • 项目类别:

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