Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

Direkt zur Navigaton springen.
Direkt zum Inhalt springen.

Navigation/Suche

"Köpfe" der aktuellen Meldungen:

Nina Höller

Nariae Baik-Schneditz

Bernhard Schwaberger

Lukas Peter Mileder

Niels Hammer

Gerhard Pichler

Roland Malli

Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid Stoffw Microb

Karbiener, M; Neuhold, C; Opriessnig, P; Prokesch, A; Bogner-Strauss, JG; Scheideler, M.
MicroRNA-30c promotes human adipocyte differentiation and co-represses PAI-1 and ALK2.
RNA Biol. 2011; 8(5):850-860 Doi: 10.4161/rna.8.5.16153 [OPEN ACCESS]
Web of Science PubMed FullText FullText_MUG

Führende Autor*innen der Med Uni Graz: Karbiener Michael
Co-Autor*innen der Med Uni Graz: Prokesch Andreas
Altmetrics:
Dimensions Citations:
Plum Analytics:
Scite (citation analytics):
Abstract:: Obesity is characterized by excessive adipose tissue mass and associated with type 2 diabetes and cardiovascular diseases. To fight obesity and its sequels, elucidating molecular events that govern adipocyte differentiation and function is of key importance. MicroRNAs (miRNAs) are a novel class of non-coding, regulatory RNAs that have been shown to regulate crucial cellular processes, including differentiation. Several studies have already assigned miRNAs to distinct functions in murine adipocyte differentiation but only a few studies did so for humans. Here, we investigated the function of miR-30c in human adipogenesis. miR-30c expression was increased during adipogenesis of human multipotent adipose-derived stem (hMADS) cells, and miR-30c overexpression enforced adipocyte marker gene induction and triglyceride accumulation. miRNA target prediction revealed two putative direct targets of miR-30c, PAI-1 (SERPINE1) and ALK2 (ACVR1, ACTRI), both inversely regulated to miR-30c during adipogenesis and responsive to miR-30c overexpression. Luciferase reporter assays confirmed PAI-1 and ALK2 as direct miR-30c targets. Moreover, reciprocal expression between miR-30c and PAI-1 could also be demonstrated in white adipose tissue of obesity mouse models, suggesting a potential physiological role of miR-30c for PAI-1 regulation in the obese state. Validating PAI-1 and ALK-2 as miR-30c mediators in adipogenesis revealed that not single silencing of PAI-1 or ALK2, but only co-silencing of both phenocopied the pro-adipogenic miR-30c effect. Thus, miR-30c can target two, so far not interconnected genes in distinct pathways, supporting the idea that miRNAs might coordinate larger regulatory networks than previously anticipated.
Find related publications in this database (using NLM MeSH Indexing): Activin Receptors, Type I - genetics Activin Receptors, Type I - metabolism; Adipocytes - cytology Adipocytes - metabolism; Adipogenesis - genetics; Adipose Tissue, White - metabolism; Animals -; Cell Differentiation -; Cell Line -; Humans -; Mesenchymal Stromal Cells - metabolism; Mice -; Mice, Obese -; Mice, Transgenic -; MicroRNAs - genetics MicroRNAs - metabolism; Multipotent Stem Cells - metabolism; Obesity -; Plasminogen Activator Inhibitor 1 - genetics Plasminogen Activator Inhibitor 1 - metabolism; RNA Interference -; RNA, Small Interfering -
Find related publications in this database (Keywords): microRNA; miR-30c; adipogenesis; adipocyte; differentiation; obesity; PAI-1; ALK2