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. 2021 Dec 24;79(1):48. doi: 10.1007/s00018-021-04049-5

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© The Author(s) 2021

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/.

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Fig. 2 — A Timeline of gene expression of SMPD1-3 in HCAECs after hyperglycemic injury, presented as 2^−ddCT vs GAPDH, n = 6. B Acidic and neutral SMase enzyme activity in HCAECs after 72 h of hyperglycemic injury, n = 5–6. C + D Immunoblotting for nSMase2 and β-Actin after 72 h of hyperglycemic injury, with quantification, n = 3. E MTT viability assay in HCAECs that were treated with lEVs from HCAECs after hyperglycemic injury, n = 6. F Flow-cytometric analysis of the induction of apoptosis in HCAECs that were treated with lEVs from HCAECs after hyperglycemic injury, (right) representative dot blots, n = 5. G MTT viability assay in HCAECs after treatment with mannitol, n = 6. H Flow-cytometric analysis of the induction of apoptosis in HCAECs that were treated with lEVs from HCAECs after osmotic injury with mannitol, n = 3. All data are presented as individual experiments with the mean ± SEM; n.s. not significant, *p < 0.05, ANOVA + Bonferoni’s multiple comparison test were used for A, E, G, and unpaired t-Test for B, D, F, H