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stemdifftm ventricular cardiomyocyte differentiation kit  (STEMCELL Technologies Inc)

 
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    STEMCELL Technologies Inc stemdifftm ventricular cardiomyocyte differentiation kit
    A Gene Set Enrichment Analysis (GSEA) of RNA-seq data showing the transcriptional perturbations induced by H3L on cardiac genes in hESCs. RNA-seq data was from Fig. . B RNA-seq analysis of cardiac lineage cells on day 3 (d3) of differentiation. Two biological replicates were applied. DEGs, differentially expressed genes. C Volcano plots showing differentially expressed genes (DEGs) induced by H3L. P < 0.05 and |log 2 (fold change) | > 0 were set as the threshold for DEGs. D Gene Ontology (GO) analysis of downregulated genes induced by H3L. E Heatmap showing H3L-downregulated genes involved in heart morphogenesis and cardiac development. FC, fold change. F RT-qPCR showing gene expression changes in cardiac lineage cells of day 3. *p < 0.05 (vs. Control). G Immunostaining of TBXT + cells in cardiac lineage cells of day 3. Green showed TBXT. Blue showed DAPI. Scale bar, 100 µm. H Flow cytometry quantification of TBXT + cells in cardiac lineage cells of day 3 from ( G ). *p < 0.05 (vs. Control). I Immunostaining of TNNT2 + cells in cardiac lineage cells of day 7. Red showed TNNT2. Blue showed DAPI. Scale bar, 200 µm. J Flow cytometry quantification of TNNT2 + cells in cardiac lineage cells of day 7 from ( I ). *p < 0.05 (vs. Control). K Flow cytometry quantification of TBXT + cells in cardiac lineage cells of day 3. IL1A was added from day 0 to day 3 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. *p < 0.05 (vs. 0 ng/ml Control). L Flow cytometry quantification of TNNT2 + cells in cardiac lineage cells of day 7. IL1A was added from day 0 to day 7 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. *p < 0.05 (vs. 0 ng/ml Control). M RT-qPCR showing relative expression of cardiogenic genes in cardiac lineage cells of day 7. IL1A was added from day 0 to day 7 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. Control, no IL1A. *p < 0.05 (vs. Control). N Gene Ontology (GO) analysis of upregulated genes induced by H3L. O GSEA analysis showing senescence and DNA damage signaling pathways. P Immunostaining of γ-H2AX + cells in cardiac lineage cells of day 3. Red showed γ-H2AX. Blue showed DAPI. Scale bar, 200 µm. Q Flow cytometry quantification of γ-H2AX + cells in cardiac lineage cells of day 3 from ( P ). *p < 0.05 (vs. Control) ( R ) Immunostaining of TUNEL + cells in cardiac lineage cells of day 3. Green showed TUNEL. Blue showed DAPI. Scale bar, 200 µm. S Flow cytometry quantification of TUNEL + cells in cardiac lineage cells of day 3. *p < 0.05 (vs. Control). T Human <t>cardiomyocytes</t> derived from hESCs were infected with lentiviruses to overexpress H3L, followed with quantification of γ-H2AX + and TUNEL + cells on 48 h later. Blank virus infection was used as Control. Flow cytometry quantification of γ-H2AX + ( U ) and TUNEL + ( V ) cardiomyocytes. *p < 0.05 (vs. Control). W H3L induces cellular injuries in human cardiac lineages via IL1A.
    Stemdifftm Ventricular Cardiomyocyte Differentiation Kit, supplied by STEMCELL Technologies Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/stemdifftm+ventricular+cardiomyocyte+differentiation+kit/pmc11339448-474-5-10?v=STEMCELL+Technologies+Inc
    Average 90 stars, based on 1 article reviews
    stemdifftm ventricular cardiomyocyte differentiation kit - by Bioz Stars, 2026-07
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    1) Product Images from "Monkeypox virus protein H3L induces injuries in human and mouse"

    Article Title: Monkeypox virus protein H3L induces injuries in human and mouse

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-024-06990-2

    A Gene Set Enrichment Analysis (GSEA) of RNA-seq data showing the transcriptional perturbations induced by H3L on cardiac genes in hESCs. RNA-seq data was from Fig. . B RNA-seq analysis of cardiac lineage cells on day 3 (d3) of differentiation. Two biological replicates were applied. DEGs, differentially expressed genes. C Volcano plots showing differentially expressed genes (DEGs) induced by H3L. P < 0.05 and |log 2 (fold change) | > 0 were set as the threshold for DEGs. D Gene Ontology (GO) analysis of downregulated genes induced by H3L. E Heatmap showing H3L-downregulated genes involved in heart morphogenesis and cardiac development. FC, fold change. F RT-qPCR showing gene expression changes in cardiac lineage cells of day 3. *p < 0.05 (vs. Control). G Immunostaining of TBXT + cells in cardiac lineage cells of day 3. Green showed TBXT. Blue showed DAPI. Scale bar, 100 µm. H Flow cytometry quantification of TBXT + cells in cardiac lineage cells of day 3 from ( G ). *p < 0.05 (vs. Control). I Immunostaining of TNNT2 + cells in cardiac lineage cells of day 7. Red showed TNNT2. Blue showed DAPI. Scale bar, 200 µm. J Flow cytometry quantification of TNNT2 + cells in cardiac lineage cells of day 7 from ( I ). *p < 0.05 (vs. Control). K Flow cytometry quantification of TBXT + cells in cardiac lineage cells of day 3. IL1A was added from day 0 to day 3 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. *p < 0.05 (vs. 0 ng/ml Control). L Flow cytometry quantification of TNNT2 + cells in cardiac lineage cells of day 7. IL1A was added from day 0 to day 7 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. *p < 0.05 (vs. 0 ng/ml Control). M RT-qPCR showing relative expression of cardiogenic genes in cardiac lineage cells of day 7. IL1A was added from day 0 to day 7 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. Control, no IL1A. *p < 0.05 (vs. Control). N Gene Ontology (GO) analysis of upregulated genes induced by H3L. O GSEA analysis showing senescence and DNA damage signaling pathways. P Immunostaining of γ-H2AX + cells in cardiac lineage cells of day 3. Red showed γ-H2AX. Blue showed DAPI. Scale bar, 200 µm. Q Flow cytometry quantification of γ-H2AX + cells in cardiac lineage cells of day 3 from ( P ). *p < 0.05 (vs. Control) ( R ) Immunostaining of TUNEL + cells in cardiac lineage cells of day 3. Green showed TUNEL. Blue showed DAPI. Scale bar, 200 µm. S Flow cytometry quantification of TUNEL + cells in cardiac lineage cells of day 3. *p < 0.05 (vs. Control). T Human cardiomyocytes derived from hESCs were infected with lentiviruses to overexpress H3L, followed with quantification of γ-H2AX + and TUNEL + cells on 48 h later. Blank virus infection was used as Control. Flow cytometry quantification of γ-H2AX + ( U ) and TUNEL + ( V ) cardiomyocytes. *p < 0.05 (vs. Control). W H3L induces cellular injuries in human cardiac lineages via IL1A.
    Figure Legend Snippet: A Gene Set Enrichment Analysis (GSEA) of RNA-seq data showing the transcriptional perturbations induced by H3L on cardiac genes in hESCs. RNA-seq data was from Fig. . B RNA-seq analysis of cardiac lineage cells on day 3 (d3) of differentiation. Two biological replicates were applied. DEGs, differentially expressed genes. C Volcano plots showing differentially expressed genes (DEGs) induced by H3L. P < 0.05 and |log 2 (fold change) | > 0 were set as the threshold for DEGs. D Gene Ontology (GO) analysis of downregulated genes induced by H3L. E Heatmap showing H3L-downregulated genes involved in heart morphogenesis and cardiac development. FC, fold change. F RT-qPCR showing gene expression changes in cardiac lineage cells of day 3. *p < 0.05 (vs. Control). G Immunostaining of TBXT + cells in cardiac lineage cells of day 3. Green showed TBXT. Blue showed DAPI. Scale bar, 100 µm. H Flow cytometry quantification of TBXT + cells in cardiac lineage cells of day 3 from ( G ). *p < 0.05 (vs. Control). I Immunostaining of TNNT2 + cells in cardiac lineage cells of day 7. Red showed TNNT2. Blue showed DAPI. Scale bar, 200 µm. J Flow cytometry quantification of TNNT2 + cells in cardiac lineage cells of day 7 from ( I ). *p < 0.05 (vs. Control). K Flow cytometry quantification of TBXT + cells in cardiac lineage cells of day 3. IL1A was added from day 0 to day 3 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. *p < 0.05 (vs. 0 ng/ml Control). L Flow cytometry quantification of TNNT2 + cells in cardiac lineage cells of day 7. IL1A was added from day 0 to day 7 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. *p < 0.05 (vs. 0 ng/ml Control). M RT-qPCR showing relative expression of cardiogenic genes in cardiac lineage cells of day 7. IL1A was added from day 0 to day 7 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. Control, no IL1A. *p < 0.05 (vs. Control). N Gene Ontology (GO) analysis of upregulated genes induced by H3L. O GSEA analysis showing senescence and DNA damage signaling pathways. P Immunostaining of γ-H2AX + cells in cardiac lineage cells of day 3. Red showed γ-H2AX. Blue showed DAPI. Scale bar, 200 µm. Q Flow cytometry quantification of γ-H2AX + cells in cardiac lineage cells of day 3 from ( P ). *p < 0.05 (vs. Control) ( R ) Immunostaining of TUNEL + cells in cardiac lineage cells of day 3. Green showed TUNEL. Blue showed DAPI. Scale bar, 200 µm. S Flow cytometry quantification of TUNEL + cells in cardiac lineage cells of day 3. *p < 0.05 (vs. Control). T Human cardiomyocytes derived from hESCs were infected with lentiviruses to overexpress H3L, followed with quantification of γ-H2AX + and TUNEL + cells on 48 h later. Blank virus infection was used as Control. Flow cytometry quantification of γ-H2AX + ( U ) and TUNEL + ( V ) cardiomyocytes. *p < 0.05 (vs. Control). W H3L induces cellular injuries in human cardiac lineages via IL1A.

    Techniques Used: RNA Sequencing, Quantitative RT-PCR, Gene Expression, Control, Immunostaining, Flow Cytometry, Concentration Assay, Expressing, Protein-Protein interactions, TUNEL Assay, Derivative Assay, Infection, Virus

    A Scheme of in vivo mouse model to study the effects of H3L in heart. Lentiviruses with control and H3L OE 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 | log 2 (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 (H3L OE ). *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 H3L OE mouse heart tissues.
    Figure Legend Snippet: A Scheme of in vivo mouse model to study the effects of H3L in heart. Lentiviruses with control and H3L OE 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 | log 2 (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 (H3L OE ). *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 H3L OE mouse heart tissues.

    Techniques Used: In Vivo, Control, Injection, RNA Sequencing, Enzyme-linked Immunosorbent Assay, Expressing, Clinical Proteomics, Marker

    A Immunostaining showing mouse P0 neonatal cardiomyocytes. TNNT2 is a specific marker of cardiomyocyte. Scale bar, 100 µm. B Statistic analysis of cell size of mouse P0 cardiomyocytes from ( A ). *p < 0.05. C Western blot showing the protein expression of NPPB in mouse cardiomyocytes. *p < 0.05. D Western blot showing the protein expression of COL1A1 in mouse cardiomyocytes. *p < 0.05. E Western blot showing the protein expression of COL3A1 in mouse cardiomyocytes. *p < 0.05.
    Figure Legend Snippet: A Immunostaining showing mouse P0 neonatal cardiomyocytes. TNNT2 is a specific marker of cardiomyocyte. Scale bar, 100 µm. B Statistic analysis of cell size of mouse P0 cardiomyocytes from ( A ). *p < 0.05. C Western blot showing the protein expression of NPPB in mouse cardiomyocytes. *p < 0.05. D Western blot showing the protein expression of COL1A1 in mouse cardiomyocytes. *p < 0.05. E Western blot showing the protein expression of COL3A1 in mouse cardiomyocytes. *p < 0.05.

    Techniques Used: Immunostaining, Marker, Western Blot, Expressing



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    A Gene Set Enrichment Analysis (GSEA) of RNA-seq data showing the transcriptional perturbations induced by H3L on cardiac genes in hESCs. RNA-seq data was from Fig. . B RNA-seq analysis of cardiac lineage cells on day 3 (d3) of differentiation. Two biological replicates were applied. DEGs, differentially expressed genes. C Volcano plots showing differentially expressed genes (DEGs) induced by H3L. P < 0.05 and |log 2 (fold change) | > 0 were set as the threshold for DEGs. D Gene Ontology (GO) analysis of downregulated genes induced by H3L. E Heatmap showing H3L-downregulated genes involved in heart morphogenesis and cardiac development. FC, fold change. F RT-qPCR showing gene expression changes in cardiac lineage cells of day 3. *p < 0.05 (vs. Control). G Immunostaining of TBXT + cells in cardiac lineage cells of day 3. Green showed TBXT. Blue showed DAPI. Scale bar, 100 µm. H Flow cytometry quantification of TBXT + cells in cardiac lineage cells of day 3 from ( G ). *p < 0.05 (vs. Control). I Immunostaining of TNNT2 + cells in cardiac lineage cells of day 7. Red showed TNNT2. Blue showed DAPI. Scale bar, 200 µm. J Flow cytometry quantification of TNNT2 + cells in cardiac lineage cells of day 7 from ( I ). *p < 0.05 (vs. Control). K Flow cytometry quantification of TBXT + cells in cardiac lineage cells of day 3. IL1A was added from day 0 to day 3 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. *p < 0.05 (vs. 0 ng/ml Control). L Flow cytometry quantification of TNNT2 + cells in cardiac lineage cells of day 7. IL1A was added from day 0 to day 7 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. *p < 0.05 (vs. 0 ng/ml Control). M RT-qPCR showing relative expression of cardiogenic genes in cardiac lineage cells of day 7. IL1A was added from day 0 to day 7 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. Control, no IL1A. *p < 0.05 (vs. Control). N Gene Ontology (GO) analysis of upregulated genes induced by H3L. O GSEA analysis showing senescence and DNA damage signaling pathways. P Immunostaining of γ-H2AX + cells in cardiac lineage cells of day 3. Red showed γ-H2AX. Blue showed DAPI. Scale bar, 200 µm. Q Flow cytometry quantification of γ-H2AX + cells in cardiac lineage cells of day 3 from ( P ). *p < 0.05 (vs. Control) ( R ) Immunostaining of TUNEL + cells in cardiac lineage cells of day 3. Green showed TUNEL. Blue showed DAPI. Scale bar, 200 µm. S Flow cytometry quantification of TUNEL + cells in cardiac lineage cells of day 3. *p < 0.05 (vs. Control). T Human <t>cardiomyocytes</t> derived from hESCs were infected with lentiviruses to overexpress H3L, followed with quantification of γ-H2AX + and TUNEL + cells on 48 h later. Blank virus infection was used as Control. Flow cytometry quantification of γ-H2AX + ( U ) and TUNEL + ( V ) cardiomyocytes. *p < 0.05 (vs. Control). W H3L induces cellular injuries in human cardiac lineages via IL1A.
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    A Gene Set Enrichment Analysis (GSEA) of RNA-seq data showing the transcriptional perturbations induced by H3L on cardiac genes in hESCs. RNA-seq data was from Fig. . B RNA-seq analysis of cardiac lineage cells on day 3 (d3) of differentiation. Two biological replicates were applied. DEGs, differentially expressed genes. C Volcano plots showing differentially expressed genes (DEGs) induced by H3L. P < 0.05 and |log 2 (fold change) | > 0 were set as the threshold for DEGs. D Gene Ontology (GO) analysis of downregulated genes induced by H3L. E Heatmap showing H3L-downregulated genes involved in heart morphogenesis and cardiac development. FC, fold change. F RT-qPCR showing gene expression changes in cardiac lineage cells of day 3. *p < 0.05 (vs. Control). G Immunostaining of TBXT + cells in cardiac lineage cells of day 3. Green showed TBXT. Blue showed DAPI. Scale bar, 100 µm. H Flow cytometry quantification of TBXT + cells in cardiac lineage cells of day 3 from ( G ). *p < 0.05 (vs. Control). I Immunostaining of TNNT2 + cells in cardiac lineage cells of day 7. Red showed TNNT2. Blue showed DAPI. Scale bar, 200 µm. J Flow cytometry quantification of TNNT2 + cells in cardiac lineage cells of day 7 from ( I ). *p < 0.05 (vs. Control). K Flow cytometry quantification of TBXT + cells in cardiac lineage cells of day 3. IL1A was added from day 0 to day 3 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. *p < 0.05 (vs. 0 ng/ml Control). L Flow cytometry quantification of TNNT2 + cells in cardiac lineage cells of day 7. IL1A was added from day 0 to day 7 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. *p < 0.05 (vs. 0 ng/ml Control). M RT-qPCR showing relative expression of cardiogenic genes in cardiac lineage cells of day 7. IL1A was added from day 0 to day 7 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. Control, no IL1A. *p < 0.05 (vs. Control). N Gene Ontology (GO) analysis of upregulated genes induced by H3L. O GSEA analysis showing senescence and DNA damage signaling pathways. P Immunostaining of γ-H2AX + cells in cardiac lineage cells of day 3. Red showed γ-H2AX. Blue showed DAPI. Scale bar, 200 µm. Q Flow cytometry quantification of γ-H2AX + cells in cardiac lineage cells of day 3 from ( P ). *p < 0.05 (vs. Control) ( R ) Immunostaining of TUNEL + cells in cardiac lineage cells of day 3. Green showed TUNEL. Blue showed DAPI. Scale bar, 200 µm. S Flow cytometry quantification of TUNEL + cells in cardiac lineage cells of day 3. *p < 0.05 (vs. Control). T Human cardiomyocytes derived from hESCs were infected with lentiviruses to overexpress H3L, followed with quantification of γ-H2AX + and TUNEL + cells on 48 h later. Blank virus infection was used as Control. Flow cytometry quantification of γ-H2AX + ( U ) and TUNEL + ( V ) cardiomyocytes. *p < 0.05 (vs. Control). W H3L induces cellular injuries in human cardiac lineages via IL1A.

    Journal: Cell Death & Disease

    Article Title: Monkeypox virus protein H3L induces injuries in human and mouse

    doi: 10.1038/s41419-024-06990-2

    Figure Lengend Snippet: A Gene Set Enrichment Analysis (GSEA) of RNA-seq data showing the transcriptional perturbations induced by H3L on cardiac genes in hESCs. RNA-seq data was from Fig. . B RNA-seq analysis of cardiac lineage cells on day 3 (d3) of differentiation. Two biological replicates were applied. DEGs, differentially expressed genes. C Volcano plots showing differentially expressed genes (DEGs) induced by H3L. P < 0.05 and |log 2 (fold change) | > 0 were set as the threshold for DEGs. D Gene Ontology (GO) analysis of downregulated genes induced by H3L. E Heatmap showing H3L-downregulated genes involved in heart morphogenesis and cardiac development. FC, fold change. F RT-qPCR showing gene expression changes in cardiac lineage cells of day 3. *p < 0.05 (vs. Control). G Immunostaining of TBXT + cells in cardiac lineage cells of day 3. Green showed TBXT. Blue showed DAPI. Scale bar, 100 µm. H Flow cytometry quantification of TBXT + cells in cardiac lineage cells of day 3 from ( G ). *p < 0.05 (vs. Control). I Immunostaining of TNNT2 + cells in cardiac lineage cells of day 7. Red showed TNNT2. Blue showed DAPI. Scale bar, 200 µm. J Flow cytometry quantification of TNNT2 + cells in cardiac lineage cells of day 7 from ( I ). *p < 0.05 (vs. Control). K Flow cytometry quantification of TBXT + cells in cardiac lineage cells of day 3. IL1A was added from day 0 to day 3 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. *p < 0.05 (vs. 0 ng/ml Control). L Flow cytometry quantification of TNNT2 + cells in cardiac lineage cells of day 7. IL1A was added from day 0 to day 7 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. *p < 0.05 (vs. 0 ng/ml Control). M RT-qPCR showing relative expression of cardiogenic genes in cardiac lineage cells of day 7. IL1A was added from day 0 to day 7 during cardiac differentiation. IL1A final concentration was 0.5 ng/ml. Control, no IL1A. *p < 0.05 (vs. Control). N Gene Ontology (GO) analysis of upregulated genes induced by H3L. O GSEA analysis showing senescence and DNA damage signaling pathways. P Immunostaining of γ-H2AX + cells in cardiac lineage cells of day 3. Red showed γ-H2AX. Blue showed DAPI. Scale bar, 200 µm. Q Flow cytometry quantification of γ-H2AX + cells in cardiac lineage cells of day 3 from ( P ). *p < 0.05 (vs. Control) ( R ) Immunostaining of TUNEL + cells in cardiac lineage cells of day 3. Green showed TUNEL. Blue showed DAPI. Scale bar, 200 µm. S Flow cytometry quantification of TUNEL + cells in cardiac lineage cells of day 3. *p < 0.05 (vs. Control). T Human cardiomyocytes derived from hESCs were infected with lentiviruses to overexpress H3L, followed with quantification of γ-H2AX + and TUNEL + cells on 48 h later. Blank virus infection was used as Control. Flow cytometry quantification of γ-H2AX + ( U ) and TUNEL + ( V ) cardiomyocytes. *p < 0.05 (vs. Control). W H3L induces cellular injuries in human cardiac lineages via IL1A.

    Article Snippet: Cardiac differentiation was induced by STEMdiffTM Ventricular Cardiomyocyte Differentiation Kit (STEMCELL Technologies) according to the manual.

    Techniques: RNA Sequencing, Quantitative RT-PCR, Gene Expression, Control, Immunostaining, Flow Cytometry, Concentration Assay, Expressing, Protein-Protein interactions, TUNEL Assay, Derivative Assay, Infection, Virus

    A Scheme of in vivo mouse model to study the effects of H3L in heart. Lentiviruses with control and H3L OE 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 | log 2 (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 (H3L OE ). *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 H3L OE mouse heart tissues.

    Journal: Cell Death & Disease

    Article Title: Monkeypox virus protein H3L induces injuries in human and mouse

    doi: 10.1038/s41419-024-06990-2

    Figure Lengend Snippet: A Scheme of in vivo mouse model to study the effects of H3L in heart. Lentiviruses with control and H3L OE 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 | log 2 (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 (H3L OE ). *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 H3L OE mouse heart tissues.

    Article Snippet: Cardiac differentiation was induced by STEMdiffTM Ventricular Cardiomyocyte Differentiation Kit (STEMCELL Technologies) according to the manual.

    Techniques: In Vivo, Control, Injection, RNA Sequencing, Enzyme-linked Immunosorbent Assay, Expressing, Clinical Proteomics, Marker

    A Immunostaining showing mouse P0 neonatal cardiomyocytes. TNNT2 is a specific marker of cardiomyocyte. Scale bar, 100 µm. B Statistic analysis of cell size of mouse P0 cardiomyocytes from ( A ). *p < 0.05. C Western blot showing the protein expression of NPPB in mouse cardiomyocytes. *p < 0.05. D Western blot showing the protein expression of COL1A1 in mouse cardiomyocytes. *p < 0.05. E Western blot showing the protein expression of COL3A1 in mouse cardiomyocytes. *p < 0.05.

    Journal: Cell Death & Disease

    Article Title: Monkeypox virus protein H3L induces injuries in human and mouse

    doi: 10.1038/s41419-024-06990-2

    Figure Lengend Snippet: A Immunostaining showing mouse P0 neonatal cardiomyocytes. TNNT2 is a specific marker of cardiomyocyte. Scale bar, 100 µm. B Statistic analysis of cell size of mouse P0 cardiomyocytes from ( A ). *p < 0.05. C Western blot showing the protein expression of NPPB in mouse cardiomyocytes. *p < 0.05. D Western blot showing the protein expression of COL1A1 in mouse cardiomyocytes. *p < 0.05. E Western blot showing the protein expression of COL3A1 in mouse cardiomyocytes. *p < 0.05.

    Article Snippet: Cardiac differentiation was induced by STEMdiffTM Ventricular Cardiomyocyte Differentiation Kit (STEMCELL Technologies) according to the manual.

    Techniques: Immunostaining, Marker, Western Blot, Expressing