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A new mammalian model system for thalidomide teratogenesis: Monodelphis domestica
Daniel Sorensen1, Amanda Sackett1, Daniel J Urban1
1School of Integrative Biology, 505 South Goodwin Avenue, University of Illinois, Urbana, IL 61801, USA.
Insights
Thalidomide causes birth defects, and opossums are a suitable mammalian model to study these effects. Opossum embryos exposed to thalidomide show similar defects and vascular disruptions as seen in humans.
Area of Science:
- Developmental biology
- Teratology
- Mammalian embryology
Background:
- Thalidomide, prescribed for leprosy, causes birth defects, posing risks to newborns in developing nations.
- The precise mechanisms of thalidomide-induced developmental disruption remain unclear.
- An appropriate mammalian model is lacking for studying thalidomide teratogenesis.
Purpose of the Study:
- To evaluate the opossum (Monodelphis domestica) as a mammalian model for thalidomide teratogenesis.
- To investigate the phenotypic similarities between human and opossum thalidomide-induced defects.
- To explore the impact of thalidomide on angiogenesis in a mammalian model.
Main Methods:
- Exposure of opossum embryos to thalidomide during critical developmental periods.
- Detailed analysis of phenotypic outcomes, including craniofacial, cardiac, and limb development.
- Assessment of vascular integrity and potential disruptions in exposed embryos.
Main Results:
- Opossum embryos exhibited a spectrum of defects (heart, craniofacial, limb) and penetrance comparable to human thalidomide exposure.
- All affected opossum embryos displayed significant vascular disruptions.
- The findings support the opossum as a relevant model for human thalidomide teratogenicity.
Conclusions:
- The opossum (Monodelphis domestica) serves as a suitable mammalian model for studying thalidomide-induced birth defects.
- Thalidomide exposure in opossums leads to developmental abnormalities and disrupts angiogenesis.
- This model offers a pathway to understanding thalidomide's teratogenic mechanisms and informing preventative strategies.
Abstract:
From 1957 to 1962, thalidomide caused birth defects in >10,000 children. While the drug was pulled from the market, thalidomide is currently prescribed to treat conditions including leprosy. As a result, a new generation of babies with thalidomide defects is being born in the developing world. This represents a serious problem, as the mechanisms by which thalidomide disrupts development remain unresolved. This lack of resolution is due, in part, to the absence of an appropriate mammalian model for thalidomide teratogenesis. We test the hypothesis that opossum (Monodelphis domestica) is well suited to model human thalidomide defects. Results suggest that opossum embryos exposed to thalidomide display a range of phenotypes (e.g., heart, craniofacial, limb defects) and penetrance similar to humans. Furthermore, all opossums with thalidomide defects exhibit vascular disruptions. Results therefore support the hypotheses that opossums make a good mammalian model for thalidomide teratogenesis, and that thalidomide can severely disrupt angiogenesis in mammals.
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