PuSH - Publication Server of Helmholtz Zentrum München: MicroRNA-26 family is required for human adipogenesis and drives characteristics of brown adipocytes.

Information

Clues to quality of journals

Open Access Policy of Helmholtz Association 2016

CC Licencences

Publication Metrics

Navigation

Home

Deutsch

EVA: Electronic Publishing

New EVA Application

Research

Advanced Search

Browse by ...

... HMGU-Authors/Consortia

... Organizational Structure

... Journal

... Publication Type

... Research Data

... Arbeitsgruppen

... Publication Year

Publication overview

Statistics

Statistics (last 5 years)

OA Publications

Publish

Submit Publication

Import publication from...

...EVA

Report missing publication

Highlights

Support & Contact

Contact persons

Help

Data protection

Helmholtz Open Science

JANE Journal Estimator

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Karbiener, M.* ; Pisani, D.F.* ; Frontini, A.* ; Oberreiter, L.M.* ; Lang, E.* ; Vegiopoulos, A.* ; Mössenböck, K.* ; Bernhardt, G.A.* ; Mayr, T.* ; Hildner, F.* ; Grillari, J.* ; Ailhaud, G.* ; Herzig, S.* ; Cinti, S.* ; Amri, E.Z.* ; Scheideler, M.*

MicroRNA-26 family is required for human adipogenesis and drives characteristics of brown adipocytes.

Stem Cells 32, 1578-1590 (2014)

DOI

PMC

Abstract
Metrics
Extra information

Adipose tissue contains thermogenic adipocytes (i.e., brown and brite/beige) that oxidize nutrients at exceptionally high rates via nonshivering thermogenesis. Its recent discovery in adult humans has opened up new avenues to fight obesity and related disorders such as diabetes. Here, we identified miR-26a and -26b as key regulators of human white and brite adipocyte differentiation. Both microRNAs are upregulated in early adipogenesis, and their inhibition prevented lipid accumulation while their overexpression accelerated it. Intriguingly, miR-26a significantly induced pathways related to energy dissipation, shifted mitochondrial morphology toward that seen in brown adipocytes, and promoted uncoupled respiration by markedly increasing the hallmark protein of brown fat, uncoupling protein 1. By combining in silico target prediction, transcriptomics, and an RNA interference screen, we identified the sheddase ADAM metallopeptidase domain 17 (ADAM17) as a direct target of miR-26 that mediated the observed effects on white and brite adipogenesis. These results point to a novel, critical role for the miR-26 family and its downstream effector ADAM17 in human adipocyte differentiation by promoting characteristics of energy-dissipating thermogenic adipocytes.

Impact Factor

Scopus SNIP

Altmetric

0.000

1.719