Abstract
Placental dysfunction underlies many complications during pregnancy, and better understanding of gene function during placentation could have considerable clinical relevance. However, the lack of a facile method for placenta-specific gene manipulation has hampered investigation of placental organogenesis and the treatment of placental dysfunction. We showed previously that transduction of fertilized mouse eggs with lentiviral vectors leads to transgene expression in both the fetus and the placenta. Here we report placenta-specific gene incorporation by lentiviral transduction of mouse blastocysts after removal of the zona pellucida. All of the placentas analyzed, but none of the fetuses, were transgenic. Application of this method substantially rescued mice deficient in Ets2, Mapk14 (also known as p38α) and Mapk1 (also known as Erk2) from embryonic lethality caused by placental defects. Ectopic expression of Mapk11 also complemented Mapk14 deficiency during placentation.
| Original language | English |
|---|---|
| Pages (from-to) | 233-237 |
| Number of pages | 5 |
| Journal | Nature Biotechnology |
| Volume | 25 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Feb 1 2007 |
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All Science Journal Classification (ASJC) codes
- Biotechnology
- Bioengineering
- Applied Microbiology and Biotechnology
- Molecular Medicine
- Biomedical Engineering
Cite this
Complementation of placental defects and embryonic lethality by trophoblast-specific lentiviral gene transfer. / Okada, Yuka; Ueshin, Yuko; Isotani, Ayako; Saito-Fujita, Tomoko; Nakashima, Hisako; Kimura, Kazushi; Mizoguchi, Akira; Ohora, Masatsugu; Mori, Yoshiko; Ogata, Masato; Oshima, Robert G.; Okabe, Masaru; Ikawa, Masahito.
In: Nature Biotechnology, Vol. 25, No. 2, 01.02.2007, p. 233-237.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Complementation of placental defects and embryonic lethality by trophoblast-specific lentiviral gene transfer
AU - Okada, Yuka
AU - Ueshin, Yuko
AU - Isotani, Ayako
AU - Saito-Fujita, Tomoko
AU - Nakashima, Hisako
AU - Kimura, Kazushi
AU - Mizoguchi, Akira
AU - Ohora, Masatsugu
AU - Mori, Yoshiko
AU - Ogata, Masato
AU - Oshima, Robert G.
AU - Okabe, Masaru
AU - Ikawa, Masahito
PY - 2007/2/1
Y1 - 2007/2/1
N2 - Placental dysfunction underlies many complications during pregnancy, and better understanding of gene function during placentation could have considerable clinical relevance. However, the lack of a facile method for placenta-specific gene manipulation has hampered investigation of placental organogenesis and the treatment of placental dysfunction. We showed previously that transduction of fertilized mouse eggs with lentiviral vectors leads to transgene expression in both the fetus and the placenta. Here we report placenta-specific gene incorporation by lentiviral transduction of mouse blastocysts after removal of the zona pellucida. All of the placentas analyzed, but none of the fetuses, were transgenic. Application of this method substantially rescued mice deficient in Ets2, Mapk14 (also known as p38α) and Mapk1 (also known as Erk2) from embryonic lethality caused by placental defects. Ectopic expression of Mapk11 also complemented Mapk14 deficiency during placentation.
AB - Placental dysfunction underlies many complications during pregnancy, and better understanding of gene function during placentation could have considerable clinical relevance. However, the lack of a facile method for placenta-specific gene manipulation has hampered investigation of placental organogenesis and the treatment of placental dysfunction. We showed previously that transduction of fertilized mouse eggs with lentiviral vectors leads to transgene expression in both the fetus and the placenta. Here we report placenta-specific gene incorporation by lentiviral transduction of mouse blastocysts after removal of the zona pellucida. All of the placentas analyzed, but none of the fetuses, were transgenic. Application of this method substantially rescued mice deficient in Ets2, Mapk14 (also known as p38α) and Mapk1 (also known as Erk2) from embryonic lethality caused by placental defects. Ectopic expression of Mapk11 also complemented Mapk14 deficiency during placentation.
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UR - http://www.scopus.com/inward/citedby.url?scp=33846871665&partnerID=8YFLogxK
U2 - 10.1038/nbt1280
DO - 10.1038/nbt1280
M3 - Article
C2 - 17220877
AN - SCOPUS:33846871665
VL - 25
SP - 233
EP - 237
JO - Nature Biotechnology
JF - Nature Biotechnology
SN - 1087-0156
IS - 2
ER -