Maternal iron deficiency perturbs embryonic cardiovascular development in mice
| Autor: | Dorota Szumska, Jack J. Miller, Magda Wolna, Aimée Jacquemot, Victor L. J. Tybulewicz, Michael Troup, Fabrice Prin, Eleni Giannoulatou, Helena Rodriguez-Caro, Eleanor M. Stuart, Emily Hardman, Jacob E Munro, Elizabeth M. C. Fisher, Samira Lakhal-Littleton, Nikita Ved, Sarah De Val, Eva Lana-Elola, Rifdat Aoidi, Jacinta I. Kalisch-Smith, Shelley Harris, Duncan B. Sparrow, Timothy J. Mohun |
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| Přispěvatelé: | Kalisch-Smith, Jacinta I. [0000-0002-5071-3805], Munro, Jacob [0000-0002-2751-0989], Miller, Jack J. [0000-0002-6258-1299], Hardman, Emily [0000-0002-3073-0309], Fisher, Elizabeth M. C. [0000-0003-2850-9936], Tybulewicz, Victor L. J. [0000-0003-2439-0798], Sparrow, Duncan B. [0000-0002-1141-6613], Apollo - University of Cambridge Repository, Kalisch-Smith, Jacinta I [0000-0002-5071-3805], Miller, Jack J [0000-0002-6258-1299], Fisher, Elizabeth MC [0000-0003-2850-9936], Tybulewicz, Victor LJ [0000-0003-2439-0798], Sparrow, Duncan B [0000-0002-1141-6613] |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Heart disease General Physics and Astronomy Physiology Aorta Thoracic Penetrance 96/35 Cardiovascular System 14 38/1 0302 clinical medicine Pregnancy Edema Myocytes Cardiac Transgenes 14/19 692/308/1426 64 Multidisciplinary Stem Cells article food and beverages Cell Differentiation Iron deficiency Iron Deficiencies Coronary Vessels humanities 3. Good health Experimental models of disease Phenotype In utero Embryogenesis Female 64/60 38/39 82/1 692/499 Signal Transduction Down syndrome Offspring Science Iron Green Fluorescent Proteins 631/136/2086 Embryonic Development Tretinoin General Biochemistry Genetics and Molecular Biology 38/91 82/80 14/1 14/32 03 medical and health sciences 14/5 medicine Genetic predisposition Animals 631/136/1425 Lymphatic Vessels business.industry Disease model Gene Expression Profiling Myocardium General Chemistry medicine.disease Embryo Mammalian Teratology Mice Inbred C57BL 030104 developmental biology Risk factors Dietary Supplements 13/51 14/63 59/57 Gene-Environment Interaction business 030217 neurology & neurosurgery Biomarkers |
| Zdroj: | Kalisch-Smith, J I, Ved, N, Szumska, D, Munro, J, Troup, M, Harris, S E, Rodriguez-Caro, H, Jacquemot, A, Miller, J J, Stuart, E M, Wolna, M, Hardman, E, Prin, F, Lana-Elola, E, Aoidi, R, Fisher, E M C, Tybulewicz, V L J, Mohun, T J, Lakhal-Littleton, S, De Val, S, Giannoulatou, E & Sparrow, D B 2021, ' Maternal iron deficiency perturbs embryonic cardiovascular development in mice ', Nature Communications, vol. 12, no. 1, 3447 . https://doi.org/10.1038/s41467-021-23660-5 Nature Communications Nature Communications, Vol 12, Iss 1, Pp 1-17 (2021) |
| DOI: | 10.1038/s41467-021-23660-5 |
| Popis: | Congenital heart disease (CHD) is the most common class of human birth defects, with a prevalence of 0.9% of births. However, two-thirds of cases have an unknown cause, and many of these are thought to be caused by in utero exposure to environmental teratogens. Here we identify a potential teratogen causing CHD in mice: maternal iron deficiency (ID). We show that maternal ID in mice causes severe cardiovascular defects in the offspring. These defects likely arise from increased retinoic acid signalling in ID embryos. The defects can be prevented by iron administration in early pregnancy. It has also been proposed that teratogen exposure may potentiate the effects of genetic predisposition to CHD through gene–environment interaction. Here we show that maternal ID increases the severity of heart and craniofacial defects in a mouse model of Down syndrome. It will be important to understand if the effects of maternal ID seen here in mice may have clinical implications for women. From mouse experiments, the authors link iron deficiency in mothers with cardiovascular defects and increased retinoic acid signalling in their offspring, and giving iron early in pregnancy can prevent most defects. |
| Databáze: | OpenAIRE |
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