Suppr超能文献

一种在缺血性心脏损伤期间进行胎儿母体干细胞转移的小鼠模型。

A mouse model for fetal maternal stem cell transfer during ischemic cardiac injury.

机构信息

Mount Sinai School of Medicine, Cardiovascular Institute, New York, New York, USA.

出版信息

Clin Transl Sci. 2012 Aug;5(4):321-8. doi: 10.1111/j.1752-8062.2012.00424.x. Epub 2012 Jun 18.

Abstract

Fetal cells enter the maternal circulation during pregnancies and can persist in blood and tissues for decades, creating a state of physiologic microchimerism. Microchimerism refers to acquisition of cells from another individual and can be due to bidirectional cell traffic between mother and fetus during pregnancy. Peripartum cardiomyopathy, a rare cardiac disorder associated with high mortality rates has the highest recovery rate amongst all etiologies of heart failure although the reason is unknown. Collectively, these observations led us to hypothesize that fetal cells enter the maternal circulation and may be recruited to the sites of myocardial disease or injury. The ability to genetically modify mice makes them an ideal system for studying the phenomenon of microchimerism in cardiac disease. Described here is a mouse model for ischemic cardiac injury during pregnancy designed to study microchimerism. Wild-type virgin female mice mated with eGFP male mice underwent ligation of the left anterior descending artery to induce a myocardial infarction at gestation day 12. We demonstrate the selective homing of eGFP cells to the site of cardiac injury without such homing to noninjured tissues suggesting the presence of precise signals sensed by fetal cells enabling them to target diseased myocardium specifically.

摘要

胎儿细胞在妊娠期间进入母体循环,并可在血液和组织中持续存在数十年,形成生理性嵌合体状态。嵌合体是指从另一个个体获得细胞,这可能是由于妊娠期间母亲和胎儿之间的双向细胞迁移。围产期心肌病是一种罕见的与高死亡率相关的心脏疾病,尽管原因不明,但它是心力衰竭所有病因中恢复率最高的。综上所述,这些观察结果使我们假设胎儿细胞进入母体循环,并可能被招募到心肌疾病或损伤部位。能够对小鼠进行基因修饰使它们成为研究心脏疾病中嵌合体现象的理想系统。这里描述的是一种在妊娠期间用于研究缺血性心脏损伤的小鼠模型,用于研究嵌合体。与 eGFP 雄性小鼠交配的野生型处女雌性小鼠在妊娠第 12 天结扎左前降支以诱导心肌梗死。我们证明了 eGFP 细胞选择性归巢到心脏损伤部位,而不会归巢到未受伤的组织,这表明胎儿细胞感知到了精确的信号,使它们能够特异性地靶向患病的心肌。

相似文献

1
A mouse model for fetal maternal stem cell transfer during ischemic cardiac injury.
Clin Transl Sci. 2012 Aug;5(4):321-8. doi: 10.1111/j.1752-8062.2012.00424.x. Epub 2012 Jun 18.
2
Fetal cells traffic to injured maternal myocardium and undergo cardiac differentiation.
Circ Res. 2012 Jan 6;110(1):82-93. doi: 10.1161/CIRCRESAHA.111.249037. Epub 2011 Nov 14.
3
Fetal cell microchimerism in the maternal heart: baby gives back.
Circ Res. 2012 Jan 6;110(1):3-5. doi: 10.1161/CIRCRESAHA.111.260299.
6
Natural history of fetal cell microchimerism during and following murine pregnancy.
J Reprod Immunol. 2005 Jun;66(1):1-12. doi: 10.1016/j.jri.2005.02.001.
7
Role of fetal stem cells in maternal tissue regeneration.
Gene Regul Syst Bio. 2007 Sep 6;1:111-5.
8
Advancing the detection of maternal haematopoietic microchimeric cells in fetal immune organs in mice by flow cytometry.
Chimerism. 2014;5(3-4):99-102. doi: 10.4161/19381956.2014.959827. Epub 2014 Oct 30.
10
Transplacental traffic after in utero mesenchymal stem cell transplantation.
Stem Cells Dev. 2010 Sep;19(9):1385-92. doi: 10.1089/scd.2009.0434.

引用本文的文献

1
Presence of fetal microchimerisms in the heart and effect on cardiac repair.
Front Cell Dev Biol. 2024 Aug 5;12:1390533. doi: 10.3389/fcell.2024.1390533. eCollection 2024.
2
Feto-maternal microchimerism: Memories from pregnancy.
iScience. 2021 Dec 29;25(1):103664. doi: 10.1016/j.isci.2021.103664. eCollection 2022 Jan 21.
3
Unravelling the biological secrets of microchimerism by single-cell analysis.
Brief Funct Genomics. 2018 Jul 1;17(4):255-264. doi: 10.1093/bfgp/elx027.
4
Multiparity improves outcomes after cerebral ischemia in female mice despite features of increased metabovascular risk.
Proc Natl Acad Sci U S A. 2017 Jul 11;114(28):E5673-E5682. doi: 10.1073/pnas.1607002114. Epub 2017 Jun 23.
5
Novel insights into the link between fetal cell microchimerism and maternal cancers.
J Cancer Res Clin Oncol. 2016 Aug;142(8):1697-704. doi: 10.1007/s00432-015-2110-3. Epub 2016 Jan 8.

本文引用的文献

1
Fetal cells traffic to injured maternal myocardium and undergo cardiac differentiation.
Circ Res. 2012 Jan 6;110(1):82-93. doi: 10.1161/CIRCRESAHA.111.249037. Epub 2011 Nov 14.
3
Fetal cells in the pregnant mouse are diverse and express a variety of progenitor and differentiated cell markers.
Biol Reprod. 2009 Jul;81(1):26-32. doi: 10.1095/biolreprod.108.074468. Epub 2009 Mar 11.
4
Notch1 signaling stimulates proliferation of immature cardiomyocytes.
J Cell Biol. 2008 Oct 6;183(1):117-28. doi: 10.1083/jcb.200806091. Epub 2008 Sep 29.
6
Fetomaternal trafficking in the mouse increases as delivery approaches and is highest in the maternal lung.
Biol Reprod. 2008 Nov;79(5):841-8. doi: 10.1095/biolreprod.108.068973. Epub 2008 Jul 16.
7
Murine maternal cell microchimerism: analysis using real-time PCR and in vivo imaging.
Biol Reprod. 2008 May;78(5):883-7. doi: 10.1095/biolreprod.107.063305. Epub 2008 Feb 6.
8
Cyclin A2 induces cardiac regeneration after myocardial infarction and prevents heart failure.
Circ Res. 2007 Jun 22;100(12):1741-8. doi: 10.1161/CIRCRESAHA.107.153544. Epub 2007 May 10.
9
Maternal neoangiogenesis during pregnancy partly derives from fetal endothelial progenitor cells.
Proc Natl Acad Sci U S A. 2007 Feb 6;104(6):1871-6. doi: 10.1073/pnas.0606490104. Epub 2007 Jan 31.
10
Bi-directional cell trafficking between mother and fetus in mouse placenta.
Placenta. 2007 Jul;28(7):639-49. doi: 10.1016/j.placenta.2006.10.006. Epub 2006 Nov 20.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验