A new mammalian model system for thalidomide teratogenesis: Monodelphis domestica

Daniel  Sorensen; Amanda Sackett; Daniel J  Urban; Jennifer  Maier; Neil Vargesson; Karen E  Sears

doi:10.1016/j.reprotox.2017.01.010

A new mammalian model system for thalidomide teratogenesis: Monodelphis domestica

Daniel Sorensen, Amanda Sackett, Daniel J Urban, Jennifer Maier, Neil Vargesson, Karen E Sears (Corresponding Author)

Medical Sciences

University of Illinois at Urbana-Champaign

Research output: Contribution to journal › Article › peer-review

9 Citations (Scopus)

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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.

Original language	English
Pages (from-to)	126-132
Number of pages	7
Journal	Reproductive Toxicology
Volume	70
Early online date	24 Jan 2017
DOIs	https://doi.org/10.1016/j.reprotox.2017.01.010
Publication status	Published - Jun 2017

Bibliographical note

We thank the members of the Sears Lab and J. Marcot for discussion of ideas presented in this manuscript, and the DAR at the University of Illinois for insights into animal husbandry. We also thank the Suarez Lab for the use of equipment. This research was supported by National Science Foundation (1257873) and University of Illinois Research Board (16056) grants to K.E.S

Keywords

teratogen
congenital birth defects
limb
angiogenesis

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Accepted Manuscript
© 2017. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
Accepted author manuscript, 1.25 MBLicence: CC BY-NC-ND

Thalidomide research guides recognition and compensation for survivors born with Thalidomide damage
Neil Vargesson (Coordinator) & Lynda Erskine (Coordinator)
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title = "A new mammalian model system for thalidomide teratogenesis: Monodelphis domestica",

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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note = "We thank the members of the Sears Lab and J. Marcot for discussion of ideas presented in this manuscript, and the DAR at the University of Illinois for insights into animal husbandry. We also thank the Suarez Lab for the use of equipment. This research was supported by National Science Foundation (1257873) and University of Illinois Research Board (16056) grants to K.E.S",

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AU - Maier, Jennifer

AU - Vargesson, Neil

AU - Sears, Karen E

N1 - We thank the members of the Sears Lab and J. Marcot for discussion of ideas presented in this manuscript, and the DAR at the University of Illinois for insights into animal husbandry. We also thank the Suarez Lab for the use of equipment. This research was supported by National Science Foundation (1257873) and University of Illinois Research Board (16056) grants to K.E.S

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N2 - 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.

AB - 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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A new mammalian model system for thalidomide teratogenesis: Monodelphis domestica

Abstract

Bibliographical note

Keywords

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Thalidomide research guides recognition and compensation for survivors born with Thalidomide damage

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