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. 2019 Nov 25;9:17451. doi: 10.1038/s41598-019-53826-7

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© The Author(s) 2019

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Long-term exposure of kisspeptin decreases (pro)insulin protein level and activates autophagy in NIT-1 cells. Representative blots (a) and mRNA levels of insulin (c) in NIT-1 cells after transfecting pcDNA3.1 + mKiss1-T2A-GFP for 72 h. Quantifications of blots and mRNA normalized by β-actin or RPL19 are shown as the means ± standard errors of the mean (n = 3). (b) Representative blots of autophagy flux marker in cultured NIT-1 cells after overexpressing Kiss1 with/without treating with bafilomycin A1 (20 nM, 3 h). Quantifications of LC3-II normalized by β-actin are shown as the means ± standard errors of the mean (n = 3), which represents autophagy flux. *Compared with level of the control; ^*p < 0.05; ^#Compared with autophagy flux of the control; ^#p < 0.05. The full-length blots are presented in Supplementary Fig. S2.