Cooperative and Independent Functions of the miR-23a~27a~24-2 Cluster in Bovine Adipocyte Adipogenesis
The cluster is an important regulator in cell metabolism. However, the cooperative and independent functions of this cluster in bovine adipocyte adipogenesis have not been elucidated. In this study, we found that expression of the cluster was induced during adipogenesis and this cluster acted as a n...
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Published in: | International journal of molecular sciences Vol. 19; no. 12; p. 3957 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Switzerland
MDPI AG
09-12-2018
MDPI |
Subjects: | |
Online Access: | Get full text |
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Summary: | The
cluster is an important regulator in cell metabolism. However, the cooperative and independent functions of this cluster in bovine adipocyte adipogenesis have not been elucidated. In this study, we found that expression of the
cluster was induced during adipogenesis and this cluster acted as a negative regulator of adipogenesis.
and
were shown to inhibit adipogenesis by directly targeting glycerol-3-phosphate acyltransferase, mitochondrial (
) and diacylglycerol O-acyltransferase 2 (
), both of which promoted adipogenesis. Meanwhile,
and
were shown to target decorin (
), glucose-6-phosphate dehydrogenase (
), and lipoprotein lipase (
), all of which repressed adipogenesis in this study. Thus, the
cluster exhibits a non-canonical regulatory role in bovine adipocyte adipogenesis. To determine how the
cluster inhibits adipogenesis while targeting anti-adipogenic genes, we identified another target gene, fibroblast growth factor 11 (
), a positive regulator of adipogenesis, that was commonly targeted by the entire
cluster. Our findings suggest that the
cluster fine-tunes the regulation of adipogenesis by targeting two types of genes with pro- or anti-adipogenic effects. This balanced regulatory role of
cluster finally repressed adipogenesis. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. |
ISSN: | 1422-0067 1661-6596 1422-0067 |
DOI: | 10.3390/ijms19123957 |