Fig. 5: H3L induce transcriptional perturbations in mouse heart. | Cell Death & Disease

Fig. 5: H3L induce transcriptional perturbations in mouse heart.

From: Monkeypox virus protein H3L induces injuries in human and mouse

Fig. 5

A Scheme of in vivo mouse model to study the effects of H3L in heart. Lentiviruses with control and H3LOE were intraperitoneally injected into one month old mouse. Two months later, heart tissues were collected for bulk RNA-seq. B ELISA assay showing protein expression level of IL1A in blood plasma from mouse heart. *p < 0.05 (vs. Control). Relative level in the Y-axis meant the read count on the absorption at 450 nm by the equipment. C Principal component analysis (PCA) of RNA-seq on mouse heart tissues. Three biological replicates were applied for RNA-seq. D Volcano plots showing differentially expressed genes (DEGs) in heart tissues induced by H3L. P < 0.05 and | log2(fold change) | > 0 were set as the threshold for DEGs. E Signaling pathway analysis of differentially expressed genes induced by H3L. The top 20 of highest ranked GO terms were presented. Pathway analysis was run on Reactome. Padj, adjusted p value. F Heatmap showing differentially expressed genes (DEGs) induced by H3L, which were involved in the Citric acid cycle and Respiratory electron transport. G Evaluation of ATP amount in mouse neonatal cardiomyocytes overexpressed with control lentivirus (Control) or H3L lentivirus (H3LOE). *p < 0.05 (vs. Control). Heatmap showing differentially expressed genes induced by H3L, which were involved in the atrial/ventricle morphogenesis (H) and aorta development (I). J RNA-seq read counts showing the expression levels of cardiac hypertrophy marker Nppb in Control and H3LOE mouse heart tissues.

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