van der Vorst, Emiel P. C.;
Pepe, Mario A. A.;
Peters, Linsey J. F.;
Haberbosch, Markus;
Jansen, Yvonne;
Naumann, Ronald;
Stathopoulos, Georgios T.;
Weber, Christian;
Bidzhekov, Kiril
Transcriptome signature of miRNA-26b KO mouse model suggests novel targets
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Media type:
E-Article
Title:
Transcriptome signature of miRNA-26b KO mouse model suggests novel targets
Contributor:
van der Vorst, Emiel P. C.;
Pepe, Mario A. A.;
Peters, Linsey J. F.;
Haberbosch, Markus;
Jansen, Yvonne;
Naumann, Ronald;
Stathopoulos, Georgios T.;
Weber, Christian;
Bidzhekov, Kiril
imprint:
Springer Science and Business Media LLC, 2021
Description:
<jats:title>Abstract</jats:title><jats:sec>
<jats:title>Background</jats:title>
<jats:p>MicroRNAs (miRNAs) are short (20–24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. One of the miRNAs that has been shown to play a role in various pathologies like cancer, neurological disorders and cardiovascular diseases is miRNA-26b. However, these studies only demonstrated rather ambiguous associations without revealing a causal relationship. Therefore, the aim of this study is to establish and validate a mouse model which enables the elucidation of the exact role of miRNA-26b in various pathologies.</jats:p>
</jats:sec><jats:sec>
<jats:title>Results</jats:title>
<jats:p>A miRNA-26b-deficient mouse model was established using homologous recombination and validated using PCR. miRNA-26b-deficient mice did not show any physiological abnormalities and no effects on systemic lipid levels, blood parameters or tissue leukocytes. Using next generation sequencing, the gene expression patterns in miRNA-26b-deficient mice were analyzed and compared to wild type controls. This supported the already suggested role of miRNA-26b in cancer and neurological processes, but also revealed novel associations of miRNA-26b with thermogenesis and allergic reactions. In addition, detailed analysis identified several genes that seem to be highly regulated by miRNA-26b, which are linked to the same pathological conditions, further confirming the role of miRNA-26b in these pathologies and providing a strong validation of our mouse model.</jats:p>
</jats:sec><jats:sec>
<jats:title>Conclusions</jats:title>
<jats:p>miRNA-26b plays an important role in various pathologies, although causal relationships still have to be established. The described mouse model of miRNA-26b deficiency is a crucial first step towards the identification of the exact role of miRNA-26b in various diseases that could identify miRNA-26b as a promising novel diagnostic or even therapeutic target in a broad range of pathologies.</jats:p>
</jats:sec>