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. 2020 Apr 28;11:163. doi: 10.1186/s13287-020-01674-y

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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. 3 — LSD1 knockdown or inhibition enhances the generation of PP2 cells. a Diagram of experimental design for d, e, and h. b Diagram of experimental design for f, g, and i. c Relative mRNA expression of pancreatic progenitor associated genes detected by real-time PCR at the end of PP2 after LSD1 knockdown (d, f). The co-expression of PDX1 with NKX6.1 was detected by immunofluorescence assay at stage 3 in control and LSD1-shRNA group (d) and control and TCP group (f), respectively. Effects of LSD1 shRNAs (e, h) and TCP (g, i) on the co-expression of PDX1 and NKX6.1 during pancreatic progenitor differentiation and quantification of the proportion of PDX1⁺/NKX6.1⁺, respectively. Data represent mean ± SEM, *p < 0.05, **p < 0.01, ***p < 0.001, two-sided student’s t test (n = 3 biologically independent samples per group)