Author
Listed:
- Mariana Schroeder
(Weizmann Institute of Science
Max Planck Institute of Psychiatry)
- Mira Jakovcevski
(Max Planck Institute of Psychiatry)
- Tamar Polacheck
(Weizmann Institute of Science
Max Planck Institute of Psychiatry)
- Yonat Drori
(Weizmann Institute of Science
Max Planck Institute of Psychiatry)
- Alessia Luoni
(Max Planck Institute of Psychiatry)
- Simone Röh
(Max Planck Institute of Psychiatry)
- Jonas Zaugg
(University of Bern
University of Bern)
- Shifra Ben-Dor
(Weizmann Institute of Science)
- Christiane Albrecht
(University of Bern
University of Bern)
- Alon Chen
(Weizmann Institute of Science
Max Planck Institute of Psychiatry)
Abstract
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.
Suggested Citation
Mariana Schroeder & Mira Jakovcevski & Tamar Polacheck & Yonat Drori & Alessia Luoni & Simone Röh & Jonas Zaugg & Shifra Ben-Dor & Christiane Albrecht & Alon Chen, 2018.
"Placental miR-340 mediates vulnerability to activity based anorexia in mice,"
Nature Communications, Nature, vol. 9(1), pages 1-15, December.
Handle:
RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03836-2
DOI: 10.1038/s41467-018-03836-2
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