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. 2016 Sep 30;7:12864. doi: 10.1038/ncomms12864

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Copyright © 2016, The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Significant increase of hlnc-MGC (human homologue of lnc-MGC), miR-379, miR-494, miR-495 and miR-377 in human MC (HMC) treated with TGF-β1 (a) or HG (b) compared with respective controls (SD or normal glucose), but not miR-882 (outside of miR-379 cluster). These increases were significantly reduced in HMC transfected with HMGC10 compared with control oligo. (c) HMGC10 mediated restoration of miR-379 cluster targets, EDEM3, ATF3, CUGBP2 and CPEB4 which were inhibited by TGF-β1 in HMC. (d) Significant increase of profibrotic genes, TGF-β1, COL1A2, COL4A1, FN1 and CTGF in HMC treated with TGF-β1 and their significant inhibition in HMC transfected with HMGC10. (e) HMGC10 mediated restoration of miR-379 cluster targets, EDEM3, ATF3, CUGBP2 and CPEB4 which were inhibited by HG in HMC. (f) Significant increase of profibrotic genes, TGF-β1, COL1A2, COL4A1, FN1 and CTGF in HMC treated with HG which was significantly inhibited by HMGC10. Results are mean+s.e. in triplicate PCRs from three independent culture experiments. *P<0.05.