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The platelet‐derived growth factor receptor alpha promoter‐directed expression of cre recombinase in mouse placenta
BACKGROUND: Numerous pathologies of pregnancy originate from placental dysfunction. It is essential to understand the functions of key genes in the placenta in order to discern the etiology of placental pathologies. A paucity of animal models that allow conditional and inducible expression of a targ...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley & Sons, Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6488356/ https://www.ncbi.nlm.nih.gov/pubmed/30843624 http://dx.doi.org/10.1002/dvdy.21 |
Sumario: | BACKGROUND: Numerous pathologies of pregnancy originate from placental dysfunction. It is essential to understand the functions of key genes in the placenta in order to discern the etiology of placental pathologies. A paucity of animal models that allow conditional and inducible expression of a target gene in the placenta is a major limitation for studying placental development and function. RESULTS: To study the platelet‐derived growth factor receptor alpha (PDGFRα)‐directed and tamoxifen‐induced Cre recombinase expression in the placenta, PDGFRα‐CreER mice were crossed with mT/mG dual‐fluorescent reporter mice. The expression of endogenous membrane‐localized enhanced green fluorescent protein (mEGFP) and/or dTomato in the placenta was examined to identify PDGFRα promoter‐directed Cre expression. Pregnant PDGFRα‐CreER;mT/mG mice were treated with tamoxifen at various gestational ages. Upon tamoxifen treatment, reporter protein mEGFP was observed in the junctional zone (JZ) and chorionic plate (CP). Furthermore, a single dose of tamoxifen was sufficient to induce the recombination. CONCLUSIONS: PDGFRα‐CreER expression is restricted to the JZ and CP of mouse placentas. PDGFRα‐CreER mice provide a useful tool to conditionally knock out or overexpress a target gene in these regions of the mouse placenta. |
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