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Berschneider, B. ; Ellwanger, D.C. ; Baarsma, H.A. ; Thiel, C.T. ; Shimbori, C.* ; White, E.S.* ; Kolb, M.* ; Neth, P.* ; Königshoff, M.

miR-92a regulates TGF-β1-induced WISP1 expression in pulmonary fibrosis.

Int. J. Biochem. Cell Biol. 53, 432-441 (2014)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Idiopathic pulmonary fibrosis (IPF) is the most common and fatal form of idiopathic interstitial pneumonia. MicroRNAs (miRNAs), short, single-stranded RNAs that regulate protein expression in a post-transcriptional manner, have recently been demonstrated to contribute to IPF pathogenesis. We have previously identified WNT1-inducible signaling pathway protein 1 (WISP1) as a highly expressed pro-fibrotic mediator in IPF, but the underlying mechanisms resulting in increased WISP1 expression, remain elusive. Here, we investigated whether WISP1 is a target of miRNA regulation. We applied a novel supervised machine learning approach, which predicted miR-30a/d and miR-92a target sites in regions of the human WISP1 3'UTR preferentially bound by the miRNA ribonucleoprotein complex. Both miRNAs were decreased in IPF samples, whereas WISP1 protein was increased. We demonstrated further that transforming growth factor (TGF)-β1-induced WISP1 expression in primary lung fibroblasts in vitro and lung homogenates in vivo. Notably, miR-30a and miR-92a reversed TGF-β1-induced WISP1 mRNA expression in lung fibroblasts. Moreover, miR-92a inhibition increased WISP1 protein expression in lung fibroblasts. An inverse relationship for WISP1 and miR-92a was found in a TGF-β1 dependent lung fibrosis model in vivo. Finally, we found significantly increased WISP1 expression in primary IPF fibroblasts, which negatively correlated with miR-92a level ex vivo. Altogether, our findings indicate a regulatory role of miR-92a for WISP1 expression in pulmonary fibrosis.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Ccn4 ; Pulmonary Fibrosis ; Wisp1 ; Mir-30 ; Mir-92a; Tissue Growth-factor; Epithelial-mesenchymal Transition; Wnt/beta-catenin Pathway; Binding-protein; Messenger-rna; Lung Fibrosis; Mir-17-92 Cluster; Beta-catenin; Genes; Sites
Sprache englisch
Veröffentlichungsjahr 2014
HGF-Berichtsjahr 2014
ISSN (print) / ISBN 1357-2725
e-ISSN 1878-5875
Zeitschrift International Journal of Biochemistry & Cell Biology, The
Quellenangaben Band: 53, Heft: , Seiten: 432-441 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort Oxford
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Lung Health and Immunity (LHI)
German Center for Lung Research (DZL)
Institute of Bioinformatics and Systems Biology (IBIS)
POF Topic(s) 30503 - Chronic Diseases of the Lung and Allergies
30202 - Environmental Health
80000 - German Center for Lung Research
30505 - New Technologies for Biomedical Discoveries
Forschungsfeld(er) Lung Research
Enabling and Novel Technologies
PSP-Element(e) G-551800-001
G-501600-006
G-501800-855
G-503700-001
PubMed ID 24953558
DOI 10.1016/j.biocel.2014.06.011
WOS ID WOS:000340340400050
Erfassungsdatum 2014-06-25
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