human ventricular cardiomyocyte line ac16  (ATCC)

Journal: bioRxiv

Article Title: Lead Exposure During Differentiation Perturbs Electrophysiological Function in iPSC-Derived Cardiomyocytes in a Cell Line-Dependent Manner

doi: 10.64898/2026.10.01.755665

Figure Lengend Snippet: Differentiation protocol and subsequent purification, with Pb exposure on the first 8 days of differentiation, purification between days 10-20, and optical mapping performed for purified cardiomyocytes 7-10 days after purification.

Article Snippet: Cardiomyocytes derived above (both control and Pb exposed) were purified once beating was visualized throughout each well (days 10-20), using the PSC-Derived Cardiomyocyte Isolation Kit (#130-110-188, Miltenyi Biotec, Bergisch Gladbach, Germany) as described. ( ) This kit employs a selective depletion strategy to enhance the cardiomyocyte purity to 98%.

Techniques: Purification

Journal: bioRxiv

Article Title: Lead Exposure During Differentiation Perturbs Electrophysiological Function in iPSC-Derived Cardiomyocytes in a Cell Line-Dependent Manner

doi: 10.64898/2026.10.01.755665

Figure Lengend Snippet: For ECC genes ATP2A2 , CACNA1C, RYR2 , and SLC8A1 and K channel subunits HERG1A and B, no significant changes were observed for purified cardiomyocytes for either female or male cells treated with 0.5 and 5 µM Pb during the first 8 days of differentiation (n = 3 per cell line per treatment; one-way ANOVA p-values for each comparison labeled on the graphs).

Article Snippet: Cardiomyocytes derived above (both control and Pb exposed) were purified once beating was visualized throughout each well (days 10-20), using the PSC-Derived Cardiomyocyte Isolation Kit (#130-110-188, Miltenyi Biotec, Bergisch Gladbach, Germany) as described. ( ) This kit employs a selective depletion strategy to enhance the cardiomyocyte purity to 98%.

Techniques: Purification, Comparison, Labeling, Gene Expression

Journal: Journal of Cardiovascular Development and Disease

Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels

doi: 10.3390/jcdd13070339

Figure Lengend Snippet: Anaesthesia device and airtight chamber system used during 5.1% sevoflurane exposure of cardiomyocyte cells.

Article Snippet: Human Cardiomyocyte Complete Media with Serum, Human Cardiomyocyte Serum-Free Media (Celprogen, Torrance, CA, USA), Trypsin–EDTA, dimethyl sulfoxide, and Dihydrorhodamine-123 (DHR 123) were procured from Sigma-Aldrich (St. Louis, MO, USA).

Techniques:

Journal: Journal of Cardiovascular Development and Disease

Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels

doi: 10.3390/jcdd13070339

Figure Lengend Snippet: ( A , B ) The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on cytosolic calcium levels in cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM, on the 20th cycle) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 3). a p ˂ 0.001 and b p ˂ 0.05 vs. control, c p ˂ 0.001 vs. SEV, d p ˂ 0.001 vs. REM, and e p ˂ 0.05 vs. SEV + REM group.

Article Snippet: Human Cardiomyocyte Complete Media with Serum, Human Cardiomyocyte Serum-Free Media (Celprogen, Torrance, CA, USA), Trypsin–EDTA, dimethyl sulfoxide, and Dihydrorhodamine-123 (DHR 123) were procured from Sigma-Aldrich (St. Louis, MO, USA).

Techniques: Control

Journal: Journal of Cardiovascular Development and Disease

Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels

doi: 10.3390/jcdd13070339

Figure Lengend Snippet: The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on apoptosis levels in cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM for 10 min) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 10). a p ˂ 0.001 vs. control, b p ˂ 0.001 vs. SEV, c p ˂ 0.005 and d p ˂ 0.001 vs. REM, and e p ˂ 0.05 vs. SEV + REM.

Article Snippet: Human Cardiomyocyte Complete Media with Serum, Human Cardiomyocyte Serum-Free Media (Celprogen, Torrance, CA, USA), Trypsin–EDTA, dimethyl sulfoxide, and Dihydrorhodamine-123 (DHR 123) were procured from Sigma-Aldrich (St. Louis, MO, USA).

Techniques: Control

Journal: Journal of Cardiovascular Development and Disease

Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels

doi: 10.3390/jcdd13070339

Figure Lengend Snippet: The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on reactive oxygen and mitochondrial depolarisation levels in cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM for 10 min) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 10). a p ˂ 0.001 and b p ˂ 0.05 vs. control, c p ˂ 0.001 vs. SEV, e p ˂ 0.001 and f p ˂ 0.05 vs. REM, and g p ˂ 0.001 vs. SEV + REM.

Article Snippet: Human Cardiomyocyte Complete Media with Serum, Human Cardiomyocyte Serum-Free Media (Celprogen, Torrance, CA, USA), Trypsin–EDTA, dimethyl sulfoxide, and Dihydrorhodamine-123 (DHR 123) were procured from Sigma-Aldrich (St. Louis, MO, USA).

Techniques: Control

Journal: Journal of Cardiovascular Development and Disease

Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels

doi: 10.3390/jcdd13070339

Figure Lengend Snippet: The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on caspase-3 and caspase-9 levels in the cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM for 10 min) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 10). a p ˂ 0.001 vs. control, b p ˂ 0.001 vs. SEV, c p ˂ 0.001 vs. REM, and d p ˂ 0.001 vs. SEV + REM.

Article Snippet: Human Cardiomyocyte Complete Media with Serum, Human Cardiomyocyte Serum-Free Media (Celprogen, Torrance, CA, USA), Trypsin–EDTA, dimethyl sulfoxide, and Dihydrorhodamine-123 (DHR 123) were procured from Sigma-Aldrich (St. Louis, MO, USA).

Techniques: Control

Journal: Journal of Cardiovascular Development and Disease

Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels

doi: 10.3390/jcdd13070339

Figure Lengend Snippet: Anaesthesia device and airtight chamber system used during 5.1% sevoflurane exposure of cardiomyocyte cells.

Article Snippet: Human cardiomyocyte cells were obtained from Celprogen Inc. (Cat.

Techniques:

Journal: Journal of Cardiovascular Development and Disease

Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels

doi: 10.3390/jcdd13070339

Figure Lengend Snippet: ( A , B ) The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on cytosolic calcium levels in cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM, on the 20th cycle) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 3). a p ˂ 0.001 and b p ˂ 0.05 vs. control, c p ˂ 0.001 vs. SEV, d p ˂ 0.001 vs. REM, and e p ˂ 0.05 vs. SEV + REM group.

Article Snippet: Human cardiomyocyte cells were obtained from Celprogen Inc. (Cat.

Techniques: Control

Journal: Journal of Cardiovascular Development and Disease

Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels

doi: 10.3390/jcdd13070339

Figure Lengend Snippet: The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on apoptosis levels in cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM for 10 min) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 10). a p ˂ 0.001 vs. control, b p ˂ 0.001 vs. SEV, c p ˂ 0.005 and d p ˂ 0.001 vs. REM, and e p ˂ 0.05 vs. SEV + REM.

Article Snippet: Human cardiomyocyte cells were obtained from Celprogen Inc. (Cat.

Techniques: Control

Journal: Journal of Cardiovascular Development and Disease

Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels

doi: 10.3390/jcdd13070339

Figure Lengend Snippet: The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on reactive oxygen and mitochondrial depolarisation levels in cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM for 10 min) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 10). a p ˂ 0.001 and b p ˂ 0.05 vs. control, c p ˂ 0.001 vs. SEV, e p ˂ 0.001 and f p ˂ 0.05 vs. REM, and g p ˂ 0.001 vs. SEV + REM.

Article Snippet: Human cardiomyocyte cells were obtained from Celprogen Inc. (Cat.

Techniques: Control

Journal: Journal of Cardiovascular Development and Disease

Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels

doi: 10.3390/jcdd13070339

Figure Lengend Snippet: The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on caspase-3 and caspase-9 levels in the cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM for 10 min) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 10). a p ˂ 0.001 vs. control, b p ˂ 0.001 vs. SEV, c p ˂ 0.001 vs. REM, and d p ˂ 0.001 vs. SEV + REM.

Article Snippet: Human cardiomyocyte cells were obtained from Celprogen Inc. (Cat.

Techniques: Control

Journal: iScience

Article Title: STEMIN- and YAP5SA-induced exosomes prevent cardiomyocyte apoptosis

doi: 10.1016/j.isci.2026.116277

Figure Lengend Snippet: STEMIN and YAP5SA upregulate anti-apoptotic miRNAs and suppress the expression of apoptotic genes in cardiomyocytes OMICS analysis shows. (A) heatmap of differentially expressed apoptotic, cell-cycle arrest, and proliferative markers in STEMIN-treated adult human primary cardiomyocytes. Apoptotic markers, including TP53, CASP6, CASP12, and BAK1, were downregulated. (B) Volcano plot shows STEMIN upregulated miRNAs, including hsa-miR-101-3p and hsa-miR-499a-5p. (C and D) GO chord plots of differentially upregulated and downregulated phenotypes (GO-terms), in STEMIN- vs. SRF-treated cardiomyocytes. (E) A heatmap of YAP5SA-treated adult human primary cardiomyocytes, showing downregulated apoptotic markers, including CASP3, CASP6, CASP9, and TP53. (F) Volcano plot shows differentially expressed miRNAs, including the upregulation of hsa-let-7c-5p, and (G and H) GO chord plots of differentially upregulated and downregulated phenotypes (GO-terms), in YAP5SA- vs. YAP1-treated cardiomyocytes.

Article Snippet: Both primary human cardiomyocytes (Celprogen) and AC16 cells (Sigma Aldrich) were validated by microscopy (showing adherent, flattened, cobble-stone like morphology, growing in a monolayer).

Techniques: Expressing

Journal: iScience

Article Title: STEMIN- and YAP5SA-induced exosomes prevent cardiomyocyte apoptosis

doi: 10.1016/j.isci.2026.116277

Figure Lengend Snippet: Exosomes isolated from STEMIN and YAP5SA-treated cardiac myocytes show the accumulation of anti-apoptotic miRNAs, which may block the expression of apoptotic markers Nanoparticle tracking analysis of exosomes secreted into culture media from AC16 cardiomyocytes transfected with (A–C), (A) Empty reagent (control), (B) STEMIN-mRNA, (C) YAP5SA-mRNA. Duplicates of ∼10 μg of secreted exosomes/sample were identified by an Orbitrap mass spectrophotometer, and following proteomic analysis, volcano plots of duplicate samples are shown for (D) STEMIN, with preferentially secreted proteins such as KRAS, RAB6B, RHOC, and HNRNPH3. (E) YAP5SA, with preferentially secreted proteins such as UBE2V2, ZEB2, RAP2C, SRM, and THYN1; they both share serpin, CNTLN1, and CTSC. OMICS analysis shows a heatmap from miR-seq of (Fi) control-, STEMIN- and YAP5SA-generated exosomes, and (Fii) differentially expressed anti-apoptotic miRNAs, and their predicted apoptotic targets determined by specific miRDB [ https://mirdb.org/ ] and IMOTA (interactive multi-omics tissue atlas [ https://ccb-web.cs.uni-saarland.de/imota/mit/ ]).

Article Snippet: Both primary human cardiomyocytes (Celprogen) and AC16 cells (Sigma Aldrich) were validated by microscopy (showing adherent, flattened, cobble-stone like morphology, growing in a monolayer).

Techniques: Isolation, Blocking Assay, Expressing, Transfection, Control, Spectrophotometry, Generated, Biomarker Discovery

Journal: iScience

Article Title: STEMIN- and YAP5SA-induced exosomes prevent cardiomyocyte apoptosis

doi: 10.1016/j.isci.2026.116277

Figure Lengend Snippet: STEMIN, YAP5SA, and their activated miRNAs block staurosporine-induced apoptosis in cardiomyocytes (A) Immunofluorescence images of STEMIN- and YAP5SA-treated cardiomyocytes. (B) Quantitative cleaved-CASP3 (FITC)/DAPI relative fluorescence bar chart from STEMIN- and YAP5SA-treated cardiomyocytes. (C) Immunofluorescence images of hsa-let-7c-5p-, miR-101-3p-, and miR-499a-5p-treated cardiomyocytes. (D) Quantitative cleaved-CASP3 (FITC)/DAPI relative fluorescence bar chart from hsa-let-7c-5p-, miR-101-3p-, and miR-499a-5p-treated cardiomyocytes. Results of assays in (A–D) were performed in triplicate ( n = 3); data are represented as mean ± SEM, and analyzed by one-way ANOVA. (E–G) Immunohistochemistry images and plot, showing 4× and 10× magnified images of cleaved-CASP3 immuno-stained tissue sections of infarcted mice hearts injected with an empty reagent and an equimolar combination (COMBO) of STEMIN + YAP5SA (white arrows showing point of injection), (F) split channel images and (G) bar chart showing the quantitative cleaved-CASP3/FITC:DAPI mean relative fluorescence. Results of assays in (E–G) were performed on seven animals: three control mice (two males, one female), four treatment mice (two males, two females). Data are represented as mean ± SEM, and analyzed by Welch test. Top and bottom vertical error bars and horizontal bars with p-values are included in the bar graphs 4B, 4D, and 4G.

Article Snippet: Both primary human cardiomyocytes (Celprogen) and AC16 cells (Sigma Aldrich) were validated by microscopy (showing adherent, flattened, cobble-stone like morphology, growing in a monolayer).

Techniques: Blocking Assay, Immunofluorescence, Fluorescence, Immunohistochemistry, Staining, Injection, Control

Journal: iScience

Article Title: STEMIN- and YAP5SA-induced exosomes prevent cardiomyocyte apoptosis

doi: 10.1016/j.isci.2026.116277

Figure Lengend Snippet: Secreted exosomes from STEMIN and YAP5SA modRNA-transfected cardiac myocytes, transferred to staurosporine-treated cardiomyocytes, hinder the expression of apoptotic markers (A–C) Immunohistochemistry images and plot, showing images of cleaved-CASP3 and TUNEL immuno-staining of fixed and permeabilized AC16 cells previously cultured with exosomes from (A) AC16-only cells, STEMIN-treated AC16 cells, and YAP5SA-treated AC16 cells, after exposure to staurosporine: split channel images of DAPI (blue), cleaved-CASP3 (green), and TUNEL (red), and (B and C) bar chart showing (B) quantitative cleaved-CASP3/FITC:DAPI and (C) TUNEL:DAPI mean relative fluorescence. Data are represented as mean ± SEM and analyzed by one-way ANOVA. Top and bottom vertical error bars and horizontal bars with p-values are included in the bar graphs 5B and 5C.

Article Snippet: Both primary human cardiomyocytes (Celprogen) and AC16 cells (Sigma Aldrich) were validated by microscopy (showing adherent, flattened, cobble-stone like morphology, growing in a monolayer).

Techniques: Transfection, Expressing, Immunohistochemistry, TUNEL Assay, Immunostaining, Cell Culture, Fluorescence