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. 2020 Sep 3;12:77. doi: 10.1186/s13098-020-00585-5

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Knockdown of KCNQ1OT1 inhibited proliferation and fibrosis and promoted apoptosis in high glucose-induced HGMCs and HRGECs. High glucose-induced HGMCs and HRGECs were transfected with si-KCNQ1OT1. a The expression of KCNQ1OT1 was detected by qRT-PCR. b, c proliferation of HGMCs and HRGECs was determined by MTT assay. d apoptosis of HGMCs and HRGECs was determined by flow cytometry assay. Apoptotic rate: Annexin positive cells/all cells. e The expression of fibrosis-related proteins was detected by western blot assay in glucose-induced HGMCs and HRGECs. N = 3, *P < 0.05