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. 2024 Oct 8;15:348. doi: 10.1186/s13287-024-03958-z

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© The Author(s) 2024

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 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/.

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Fig. 2 — VIP induces secretory cell differentiation in organoids by activating the p38 MAPK pathway. A Experimental setup and inhibitors with signaling targets. B qPCR analysis of the secretory differentiation marker Lyz1 in VIP-treated organoids in the presence of inhibitors targeting potential downstream signaling pathways. n = 8 (VIP), n = 4 (all other groups). C Western blot analysis showing p38 MAPK pathway activation upon VIP treatment (n = 8 per group), full-length blots are shown in Fig. S5. D, E Quantification of LYZ1 + cells per organoid revealed by immunofluorescent analysis following indicated inhibitor treatments. n = 4 (Control; VIP), n = 5 (VIP + SB202190) in (D), n = 10 (Control), n = 12 (VIP), n = 9 (VIP + PD98059), n = 4 (VIP + BMS-345541) in (E). *p < 0.05, **p < 0.01. Data are shown as means ± SEM, n = number of biological replicates. Statistical analysis was performed by paired Student’s t-test in (C), one-way ANOVA with Tukey's multiple comparisons test in (B, D), and Mixed effects with Dunnett's multiple comparisons test in (E)