慢性社会心理压力影响小鼠卵巢中的胰岛素样生长因子1及其受体

IF 2.1
Tatyana Igonina, Daria Lebedeva, Anton Tsybko, Irina Rozhkova, Tatyana Babochkina, Alisa Levinson, Sergei Amstislavsky
{"title":"慢性社会心理压力影响小鼠卵巢中的胰岛素样生长因子1及其受体","authors":"Tatyana Igonina, Daria Lebedeva, Anton Tsybko, Irina Rozhkova, Tatyana Babochkina, Alisa Levinson, Sergei Amstislavsky","doi":"10.1071/RD24101","DOIUrl":null,"url":null,"abstract":"<p><p>Context Chronic psychosocial stress negatively affects folliculogenesis and oogenesis. Intraovarian mechanisms mediating these effects are poorly understood. Aims This work aimed to find out how chronic psychosocial stress affects ovarian IGF1 and its receptor (IGF1R), as well as Igf1 and Igf1r gene expression in cumulus-oocyte complexes (COCs). It also aimed to address possible protective effects of gonadotropin stimulation on IGF1 ovarian signalling. Methods Female CD1 mice experienced chronic psychosocial stress of 11-day isolation followed by overcrowding for 10days. To verify the model, blood corticosterone levels and the quality of oocytes were evaluated in stressed females. The levels of IGF1/IGF1R, blood IGF1 concentration, and expression of Igf1 /Igf1r in the ovaries were compared in stressed and unstressed females. Key results Psychosocial stress caused an elevation of corticosterone level, which was alleviated by gonadotropin treatment. The stressed mice showed a decreased IGF1 level in the ovaries and a decreased expression of Igf1 and Igf1r in COCs. In the unstressed females, gonadotropin injection decreased the expression of Igf1 and Igf1r ; in the stressed females, the same treatment increased Igf1r expression. Neither stress nor ovarian stimulation with gonadotropins affected the serum IGF1 level. Conclusions Psychosocial stress suppresses IGF1 signalling in the ovaries. Gonadotropin treatment modulates these effects differently in stressed and unstressed animals. Implications The results may have translational value for human reproduction. Ovarian IGF1 can be considered a candidate for further improvement of IVF results in women under conditions of chronic stress.</p>","PeriodicalId":516117,"journal":{"name":"Reproduction, fertility, and development","volume":"36 ","pages":""},"PeriodicalIF":2.1000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Chronic psychosocial stress affects insulin-like growth factor 1 and its receptors in mouse ovaries.\",\"authors\":\"Tatyana Igonina, Daria Lebedeva, Anton Tsybko, Irina Rozhkova, Tatyana Babochkina, Alisa Levinson, Sergei Amstislavsky\",\"doi\":\"10.1071/RD24101\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Context Chronic psychosocial stress negatively affects folliculogenesis and oogenesis. Intraovarian mechanisms mediating these effects are poorly understood. Aims This work aimed to find out how chronic psychosocial stress affects ovarian IGF1 and its receptor (IGF1R), as well as Igf1 and Igf1r gene expression in cumulus-oocyte complexes (COCs). It also aimed to address possible protective effects of gonadotropin stimulation on IGF1 ovarian signalling. Methods Female CD1 mice experienced chronic psychosocial stress of 11-day isolation followed by overcrowding for 10days. To verify the model, blood corticosterone levels and the quality of oocytes were evaluated in stressed females. The levels of IGF1/IGF1R, blood IGF1 concentration, and expression of Igf1 /Igf1r in the ovaries were compared in stressed and unstressed females. Key results Psychosocial stress caused an elevation of corticosterone level, which was alleviated by gonadotropin treatment. The stressed mice showed a decreased IGF1 level in the ovaries and a decreased expression of Igf1 and Igf1r in COCs. In the unstressed females, gonadotropin injection decreased the expression of Igf1 and Igf1r ; in the stressed females, the same treatment increased Igf1r expression. Neither stress nor ovarian stimulation with gonadotropins affected the serum IGF1 level. Conclusions Psychosocial stress suppresses IGF1 signalling in the ovaries. Gonadotropin treatment modulates these effects differently in stressed and unstressed animals. Implications The results may have translational value for human reproduction. Ovarian IGF1 can be considered a candidate for further improvement of IVF results in women under conditions of chronic stress.</p>\",\"PeriodicalId\":516117,\"journal\":{\"name\":\"Reproduction, fertility, and development\",\"volume\":\"36 \",\"pages\":\"\"},\"PeriodicalIF\":2.1000,\"publicationDate\":\"2024-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Reproduction, fertility, and development\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1071/RD24101\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Reproduction, fertility, and development","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1071/RD24101","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

背景 慢性社会心理压力会对卵泡生成和卵子生成产生负面影响。卵巢内介导这些影响的机制尚不清楚。目的 本研究旨在了解慢性社会心理压力如何影响卵巢IGF1及其受体(IGF1R),以及积液-卵母细胞复合体(COCs)中Igf1和Igf1r基因的表达。研究还旨在探讨促性腺激素刺激对 IGF1 卵巢信号的可能保护作用。方法 雌性 CD1 小鼠经历了 11 天隔离和 10 天拥挤的慢性社会心理应激。为了验证该模型,对应激雌鼠的血液皮质酮水平和卵母细胞质量进行了评估。比较了应激雌鼠和非应激雌鼠卵巢中IGF1/IGF1R的水平、血液中IGF1的浓度和Igf1/Igf1r的表达。主要结果 社会心理应激导致皮质酮水平升高,而促性腺激素治疗可缓解这一现象。应激小鼠卵巢中的 IGF1 水平下降,COC 中的 Igf1 和 Igf1r 表达减少。在未受应激的雌性小鼠中,注射促性腺激素会降低Igf1和Igf1r的表达;在受应激的雌性小鼠中,同样的处理会增加Igf1r的表达。压力和促性腺激素对卵巢的刺激都不会影响血清 IGF1 的水平。结论 社会心理压力会抑制卵巢中的 IGF1 信号。促性腺激素治疗对应激和非应激动物的这些影响有不同的调节作用。意义 这些结果可能对人类生殖具有转化价值。卵巢IGF1可被认为是进一步改善长期处于压力下的女性试管婴儿结果的候选因子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Chronic psychosocial stress affects insulin-like growth factor 1 and its receptors in mouse ovaries.

Context Chronic psychosocial stress negatively affects folliculogenesis and oogenesis. Intraovarian mechanisms mediating these effects are poorly understood. Aims This work aimed to find out how chronic psychosocial stress affects ovarian IGF1 and its receptor (IGF1R), as well as Igf1 and Igf1r gene expression in cumulus-oocyte complexes (COCs). It also aimed to address possible protective effects of gonadotropin stimulation on IGF1 ovarian signalling. Methods Female CD1 mice experienced chronic psychosocial stress of 11-day isolation followed by overcrowding for 10days. To verify the model, blood corticosterone levels and the quality of oocytes were evaluated in stressed females. The levels of IGF1/IGF1R, blood IGF1 concentration, and expression of Igf1 /Igf1r in the ovaries were compared in stressed and unstressed females. Key results Psychosocial stress caused an elevation of corticosterone level, which was alleviated by gonadotropin treatment. The stressed mice showed a decreased IGF1 level in the ovaries and a decreased expression of Igf1 and Igf1r in COCs. In the unstressed females, gonadotropin injection decreased the expression of Igf1 and Igf1r ; in the stressed females, the same treatment increased Igf1r expression. Neither stress nor ovarian stimulation with gonadotropins affected the serum IGF1 level. Conclusions Psychosocial stress suppresses IGF1 signalling in the ovaries. Gonadotropin treatment modulates these effects differently in stressed and unstressed animals. Implications The results may have translational value for human reproduction. Ovarian IGF1 can be considered a candidate for further improvement of IVF results in women under conditions of chronic stress.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信