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Argonaute2 Mediates Compensatory Expansion of the Pancreatic β Cell

Tattikota, Sudhir G. and Rathjen, Thomas and McAnulty, Sarah J. and Wessels, Hans-Hermann and Akerman, Ildem and van de Bunt, Martijn and Hausser, Jean and Esguerra, Jonathan L. S. and Musahl, Anne and Pandey, Amit K. and You, Xintian and Chen, Wei and Herrera, Pedro L. and Johnson, Paul R. and O'Carroll, Donal and Eliasson, Lena and Zavolan, Mihaela and Gloyn, Anna L. and Ferrer, Jorge and Shalom-Feuerstein, Ruby and Aberdam, Daniel and Poy, Matthew N.. (2013) Argonaute2 Mediates Compensatory Expansion of the Pancreatic β Cell. Cell metabolism, Vol. 19, H. 1. pp. 122-134.

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Official URL: http://edoc.unibas.ch/dok/A6212231

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Abstract

Pancreatic β cells adapt to compensate for increased metabolic demand during insulin resistance. Although the microRNA pathway has an essential role in β cell proliferation, the extent of its contribution is unclear. Here, we report that miR-184 is silenced in the pancreatic islets of insulin-resistant mouse models and type 2 diabetic human subjects. Reduction of miR-184 promotes the expression of its target Argonaute2 (Ago2), a component of the microRNA-induced silencing complex. Moreover, restoration of miR-184 in leptin-deficient ob/ob mice decreased Ago2 and prevented compensatory β cell expansion. Loss of Ago2 during insulin resistance blocked β cell growth and relieved the regulation of miR-375-targeted genes, including the growth suppressor Cadm1. Lastly, administration of a ketogenic diet to ob/ob mice rescued insulin sensitivity and miR-184 expression and restored Ago2 and β cell mass. This study identifies the targeting of Ago2 by miR-184 as an essential component of the compensatory response to regulate proliferation according to insulin sensitivity.
Faculties and Departments:05 Faculty of Science > Departement Biozentrum > Computational & Systems Biology > Bioinformatics (Zavolan)
UniBasel Contributors:Zavolan, Mihaela and Hausser, Jean
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:Cell Press
ISSN:1550-4131
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:31 Jan 2014 09:51
Deposited On:31 Jan 2014 09:51

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