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. 2024 Aug 27;14:19899. doi: 10.1038/s41598-024-70911-8

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 5 — Prenatal vitamin D deficiency alters cellular compositions of the embryonic liver, suggesting immune cell proportion changes start during development. (a) UMAP representation of single-cell RNA-seq gene expression data and cellular lineage identification of E14.5 fetal liver (n = 3 per group). (b) The boxplots indicate prenatal vitamin D deficiency alters cellular compositions of E14.5 fetal liver. (c) Genes downregulated in VDD E14.5 fetal liver are enriched in the genes regulated by hematopoietic transcription factors. (d) Treating HPC7 cells with 1-alpha-25-dihydroxyvitamin D₃ significantly increases gene expression levels of Erg and Lmo2, suggesting these genes are regulated by VDR (n = 3 per treatment group).