دورية أكاديمية
Variations in maternal vitamin A intake modifies phenotypes in a mouse model of 22q11.2 deletion syndrome.
| العنوان: | Variations in maternal vitamin A intake modifies phenotypes in a mouse model of 22q11.2 deletion syndrome. |
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| المؤلفون: | Yitsege G; Department of Anatomy and Cell Biology, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.; Institute for Neuroscience, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.; Center for Genetic Medicine, Children's Research Institute, Children's National Medical Center, Washington, District of Columbia, USA., Stokes BA; Center for Neuroscience Research, Children's Research Institute, Children's National Medical Center, Washington, District of Columbia, USA.; Center for Genetic Medicine, Children's Research Institute, Children's National Medical Center, Washington, District of Columbia, USA., Sabatino JA; Department of Anatomy and Cell Biology, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.; Institute for Neuroscience, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA., Sugrue KF; Center for Neuroscience Research, Children's Research Institute, Children's National Medical Center, Washington, District of Columbia, USA.; Center for Genetic Medicine, Children's Research Institute, Children's National Medical Center, Washington, District of Columbia, USA., Banyai G; Department of Anatomy and Cell Biology, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.; Institute for Neuroscience, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.; Center for Neuroscience Research, Children's Research Institute, Children's National Medical Center, Washington, District of Columbia, USA., Paronett EM; Department of Anatomy and Cell Biology, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.; Institute for Neuroscience, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA., Karpinski BA; Department of Anatomy and Cell Biology, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.; Institute for Neuroscience, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA., Maynard TM; Department of Anatomy and Cell Biology, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.; Institute for Neuroscience, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.; Fralin Biomedical Research Institute at Virginia Tech Carilion School of Medicine, Roanoke, Virginia, USA., LaMantia AS; Department of Anatomy and Cell Biology, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.; Institute for Neuroscience, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.; Fralin Biomedical Research Institute at Virginia Tech Carilion School of Medicine, Roanoke, Virginia, USA.; Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia, USA., Zohn IE; Institute for Neuroscience, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.; Center for Neuroscience Research, Children's Research Institute, Children's National Medical Center, Washington, District of Columbia, USA.; Center for Genetic Medicine, Children's Research Institute, Children's National Medical Center, Washington, District of Columbia, USA. |
| المصدر: | Birth defects research [Birth Defects Res] 2020 Oct; Vol. 112 (16), pp. 1194-1208. Date of Electronic Publication: 2020 May 20. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural |
| اللغة: | English |
| بيانات الدورية: | Publisher: John Wiley & Sons, Inc Country of Publication: United States NLM ID: 101701004 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2472-1727 (Electronic) NLM ISO Abbreviation: Birth Defects Res Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Hoboken, N.J. : John Wiley & Sons, Inc. |
| مواضيع طبية MeSH: | DiGeorge Syndrome*, Animals ; Deglutition ; Disease Models, Animal ; Mice ; Phenotype ; Vitamin A |
| مستخلص: | Background: Vitamin A regulates patterning of the pharyngeal arches, cranial nerves, and hindbrain that are essential for feeding and swallowing. In the LgDel mouse model of 22q11.2 deletion syndrome (22q11DS), morphogenesis of multiple structures involved in feeding and swallowing are dysmorphic. We asked whether changes in maternal dietary Vitamin A intake can modify cranial nerve, hindbrain and pharyngeal arch artery development in the embryo as well as lung pathology that can be a sign of aspiration dysphagia in LgDel pups. Methods: Three defined amounts of vitamin A (4, 10, and 16 IU/g) were provided in the maternal diet. Cranial nerve, hindbrain and pharyngeal arch artery development was evaluated in embryos and inflammation in the lungs of pups to determine the impact of altering maternal diet on these phenotypes. Results: Reduced maternal vitamin A intake improved whereas increased intake exacerbated lung inflammation in LgDel pups. These changes were accompanied by increased incidence and/or severity of pharyngeal arch artery and cranial nerve V (CN V) abnormalities in LgDel embryos as well as altered expression of Cyp26b1 in the hindbrain. Conclusions: Our studies demonstrate that variations in maternal vitamin A intake can influence the incidence and severity of phenotypes in a mouse model 22q11.2 deletion syndrome. (© 2020 The Authors. Birth Defects Research published by Wiley Periodicals, LLC.) |
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| معلومات مُعتمدة: | P01 HD083157 United States HD NICHD NIH HHS; R21 HD090623 United States HD NICHD NIH HHS; U54 HD090257 United States HD NICHD NIH HHS |
| فهرسة مساهمة: | Keywords: 22q11.2 deletion syndrome; Dysphagia; Gene-environment interaction; Retinoid acid; vitamin A |
| المشرفين على المادة: | 11103-57-4 (Vitamin A) |
| تواريخ الأحداث: | Date Created: 20200521 Date Completed: 20210818 Latest Revision: 20231112 |
| رمز التحديث: | 20231112 |
| مُعرف محوري في PubMed: | PMC7586978 |
| DOI: | 10.1002/bdr2.1709 |
| PMID: | 32431076 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 2472-1727 |
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| DOI: | 10.1002/bdr2.1709 |