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. 2021 Jan 26;7:24. doi: 10.1038/s41420-020-00379-8

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© The Author(s) 2021

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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Fig. 7 — a, b JEG-3 cells infected with 0.1 MOI of r-MRV for 48 h showed significant increase in apoptosis as evidenced by caspase 3/7 activity and percent apoptotic nuclear compared to uninfected vehicle treatment. ZIKV-induced placental trophoblast apoptosis were significantly prevented in JEG-3 cells infected with 0.1 MOI of r-MRV and IREi (STF-083010, IRE1α inhibitor), JNKi (SP600125, JNK inhibitor), or ZVAD (Z-VAD-fmk, pan caspase inhibitor) treatment, respectively. However, ZIKV infection and treatment of Sal (Salubrinal, eIF2α dephosphorylation inhibitor) did not prevent trophoblast apoptosis. c, d HTR-8 cells infected with 0.1 MOI of r-MRV for 72 h showed a dramatic increase in biochemical markers of apoptosis compared to uninfected vehicle cells. ZIKV-induced placental trophoblast apoptosis were significantly prevented in HTR-8 cells infected with 0.1 MOI of r-MRV and Sal (Salubrinal, eIF2α dephosphorylation inhibitor), JNKi (SP600125, JNK inhibitor), or ZVAD (Z-VAD-fmk, pan caspase inhibitor) treatment, respectively. However, ZIKV infection and IRE inhibition (STF-083010, IRE1α inhibitor) or p38 inhibition treatment does not prevent ZIKV-induced trophoblast apoptosis. e JAR cells infected with 0.1 MOI r-MRV 48 h postinfection showed activation of caspase 3/7 when compared to vehicle cells. Sal (Salubrinal, eIF2α dephosphorylation inhibitor), JNKi (SP600125, JNK inhibitor), or ZVAD (Z-VAD-fmk, pan caspase inhibitor) treatment in infected cells inhibited caspase 3/7 activation while p38 inhibition significantly increased caspase 3/7 activation. Each value presents mean ± SEM of (n = 4) for caspase 3/7 activity and n = 3 for percent apoptotic nuclei, *P < 0.05 compared to uninfected vehicle cells; ^#P < 0.05 compared to ZIKV infected cells; statistical comparison by ANOVA with posthoc Bonferroni correction.