Placental miR-340 mediates vulnerability to activity based anorexia in mice

Schroeder, Mariana; Jakovcevski, Mira; Polacheck, Tamar; Drori, Yonat; Luoni, Alessia; Roeh, Simone; Zaugg, Jonas; Ben-Dor, Shifra; Albrecht, Christiane; Chen, Alon

doi:10.1038/s41467-018-03836-2

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Placental miR-340 mediates vulnerability to activity based anorexia in mice

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Schroeder, Mariana
Dept. Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Max Planck Society;
external;

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Jakovcevski, Mira
Dept. Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Max Planck Society;

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Polacheck, Tamar
Dept. Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Max Planck Society;
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Drori, Yonat
Dept. Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Max Planck Society;
external;

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Luoni, Alessia
Dept. Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Max Planck Society;

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Roeh, Simone
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

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Chen, Alon
Dept. Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Max Planck Society;
external;

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Zitation

Schroeder, M., Jakovcevski, M., Polacheck, T., Drori, Y., Luoni, A., Roeh, S., et al. (2018). Placental miR-340 mediates vulnerability to activity based anorexia in mice. NATURE COMMUNICATIONS, 9: 1596. doi:10.1038/s41467-018-03836-2.

Zitierlink: https://hdl.handle.net/21.11116/0000-0002-5E7A-D

Zusammenfassung

Anorexia nervosa (AN) is a devastating eating disorder characterized by self-starvation that mainly affects women. Its etiology is unknown, which impedes successful treatment options leading to a limited chance of full recovery. Here, we show that gestation is a vulnerable window that can influence the predisposition to AN. By screening placental microRNA expression of naive and prenatally stressed (PNS) fetuses and assessing vulnerability to activity-based anorexia (ABA), we identify miR-340 as a sexually dimorphic regulator involved in prenatal programming of ABA. PNS caused gene-body hypermethylation of placental miR-340, which is associated with reduced miR-340 expression and increased protein levels of several target transcripts, GR, Cry2 and H3F3b. MiR-340 is linked to the expression of several nutrient transporters both in mice and human placentas. Using placenta-specific lentiviral transgenes and embryo transfer, we demonstrate the key role miR-340 plays in the mechanism involved in early life programming of ABA.