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

Schroeder, Mariana; Jakovcevski, Mira; Polacheck, Tamar; Drori, Yonat; Luoni, Alessia; Röh, Simone; Zaugg, Jonas; Ben-Dor, Shifra; Albrecht, Christiane; Chen, Alon (2018). Placental miR-340 mediates vulnerability to activity based anorexia in mice. Nature communications, 9(1), p. 1596. Nature Publishing Group 10.1038/s41467-018-03836-2

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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.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Other Institutions > NCCR TransCure
04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Biochemistry and Molecular Medicine

UniBE Contributor:

Albrecht, Christiane

Subjects:

500 Science > 570 Life sciences; biology
600 Technology > 610 Medicine & health

ISSN:

2041-1723

Publisher:

Nature Publishing Group

Language:

English

Submitter:

Barbara Järmann-Bangerter

Date Deposited:

27 Sep 2018 11:06

Last Modified:

30 Sep 2018 02:30

Publisher DOI:

10.1038/s41467-018-03836-2

PubMed ID:

29686286

BORIS DOI:

10.7892/boris.120136

URI:

https://boris.unibe.ch/id/eprint/120136

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