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Tattikota, S.G.* ; Rathjen, T.* ; Hausser, J.* ; Khedkar, A.* ; Kabra, U.D. ; Pandey, V.K.* ; Sury, M.* ; Wessels, H.H.* ; Mollet, I.G.* ; Eliasson, L.* ; Selbach, M.* ; Zinzen, R.P.* ; Zavolan, M.* ; Kadener, S.* ; Tschöp, M.H. ; Jastroch, M. ; Friedländer, M.R.* ; Poy, M.N.*

MiR-184 regulates pancreatic β-cell function according to glucose metabolism.

J. Biol. Chem. 290, 20284-20294 (2015)
Verlagsversion Postprint Forschungsdaten DOI PMC
Open Access Gold
In response to fasting or hyperglycemia, the pancreatic β-cell alters its output of secreted insulin; however the pathways governing this adaptive response are not entirely established. While the precise role of microRNAs (miRNAs) is also unclear, a recurring theme emphasizes their function in cellular stress responses. We recently showed that miR-184, an abundant miRNA in the β-cell, regulates compensatory proliferation and secretion during insulin resistance. Consistent with previous studies showing miR-184 suppresses insulin release, expression of this miRNA was increased in islets after fasting, demonstrating an active role in the β-cell as glucose levels lower and the insulin demand ceases. Additionally, miR-184 was negatively regulated upon administration of a sucrose-rich diet in Drosophila demonstrating strong conservation of this pathway through evolution. Furthermore, miR-184 and its target Argonaute2 (Ago2) remained inversely correlated as concentrations of extracellular glucose increased, underlining a functional relationship between this miRNA and its targets. Lastly, restoration of Ago2 in the presence of miR-184 rescued suppression of miR-375-targeted genes suggesting these genes act in a coordinated manner during changes in the metabolic context. Together, these results highlight the adaptive role of miR-184 according to glucose metabolism and suggest the regulatory role of this miRNA in energy homeostasis is highly conserved.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Argonaute ; Beta Cell (b-cell) ; Glucose Metabolism ; Insulin ; Insulin Secretion ; Microrna (mirna) ; Microrna Mechanism ; Pancreatic Islet; Insulin-secretion; In-vivo; Drosophila; Protein; Stress; Replication; Micrornas; Reveals; Differentiation; Proliferation
Sprache englisch
Veröffentlichungsjahr 2015
HGF-Berichtsjahr 2015
ISSN (print) / ISBN 0021-9258
e-ISSN 1083-351X
Zeitschrift Journal of Biological Chemistry, The
Quellenangaben Band: 290, Heft: 33, Seiten: 20284-20294 Artikelnummer: , Supplement: ,
Verlag American Society for Biochemistry and Molecular Biology
Verlagsort Bethesda
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
POF Topic(s) 30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502200-001
PubMed ID 26152724
DOI 10.1074/jbc.M115.658625
WOS ID WOS:000359608900028
Erfassungsdatum 2015-08-05
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