Journal: Scientific reports

Article Title: ETV1 activates a rapid conduction transcriptional program in rodent and human cardiomyocytes.

doi: 10.1038/s41598-018-28239-7

Figure Lengend Snippet: Figure 2. Cardiomyocyte-specific knockout of ETV1 slows atrial and His-Purkinje system conduction. Etv1flox/

Article Snippet: P1 NRVM heart lysates were purified using Miltenyi Biotec rat neonatal cardiomyocyte isolation kit (Miltenyi Biotec, 130–105–420) according to the manufacture’s protocol.

Techniques: Knock-Out

Journal: Scientific reports

Article Title: ETV1 activates a rapid conduction transcriptional program in rodent and human cardiomyocytes.

doi: 10.1038/s41598-018-28239-7

Figure Lengend Snippet: Figure 3. Cardiomyocyte deletion of ETV1 resulted in decreased expression of fast conduction genes in atrial and His-Purkinje system (HPS) myocytes. (A) Quantitative RT-PCR of fast conduction gene RNA levels (normalized to Gapdh) comparing 10–12-week-old Etv1 WT (Etv1flox/flox) and Etv1 cKO (Etv1flox/flox, Myh6- Cre) FACS-purified ventricular, atrial, and Purkinje myocytes. Relative Nkx2–5, Gja5, and Scn5a expression displayed versus control, Etv1 WT (n = 4). (B) Immunoblot assessment of Etv1 WT and Etv1 cKO atrial tissue lysates detecting NKX2–5, Cx40, NaV1.5, and Vinculin (loading control). (C) Protein level densitometric quantification (normalized to vinculin), displayed relative to Etv1 WT (n = 5). (D) Immunofluorescence evaluation of NKX2–5, Cx40, and NaV1.5 expression in 10-week-old Etv1 WT and Etv1 cKO atria/ventricular sections. (E) Immunofluorescence evaluation of NKX2–5, Cx40, and NaV1.5 expression in 10-week-old Etv1 WT and Etv1 cKO HPS sections. Positive CNTN2 expression identified HPS cells. Nuclei were identified by DAPI (blue). LA, left atria; LV, left ventricle. Data represent mean ± SEM. *P < 0.05, 2-tailed Student’s t test. Scale bars: 50 um.

Article Snippet: P1 NRVM heart lysates were purified using Miltenyi Biotec rat neonatal cardiomyocyte isolation kit (Miltenyi Biotec, 130–105–420) according to the manufacture’s protocol.

Techniques: Expressing, Quantitative RT-PCR, Purification, Control, Western Blot, Immunofluorescence

Journal: Scientific reports

Article Title: ETV1 activates a rapid conduction transcriptional program in rodent and human cardiomyocytes.

doi: 10.1038/s41598-018-28239-7

Figure Lengend Snippet: Figure 5. ETV1 regulates the diversity of sodium channel biophysical properties between ventricular, atrial, and Purkinje myocytes. Whole-cell patch clamp data from dissociated cardiomyocytes (ventricular, right atrial, Purkinje myocytes) using 10–12 week-old Etv1 WT (Etv1flox/flox) and Etv1 cKO (Etv1flox/flox, Myh6-Cre) mice in a Cntn2-EGFP background (n = 4). (A) Comparison of sodium current–voltage (I–V) relationship. Maximum conductance was calculated to assess significant differences among experimental groups. (B) Voltage dependence of steady-state activation. Voltage at half activation (V0.5, activation) was calculated to assess significant differences among experimental groups. (C) Voltage dependence of steady-state inactivation. Voltage at half inactivation (V0.5, inactivation) was calculated to assess significant differences among experimental groups. (D) Time course of recovery from inactivation. Tau of recovery (τrecovery) was calculated to assess significant differences among experimental groups. Number of cells analyzed per cell type (ventricle, right atria, Purkinje) included in each graph legend. Patch clamp protocol diagrams are included for each endpoint. Data represent mean ± SEM. *P < 0.05, 1-way ANOVA.

Article Snippet: P1 NRVM heart lysates were purified using Miltenyi Biotec rat neonatal cardiomyocyte isolation kit (Miltenyi Biotec, 130–105–420) according to the manufacture’s protocol.

Techniques: Patch Clamp, Comparison, Activation Assay

Journal: Scientific reports

Article Title: ETV1 activates a rapid conduction transcriptional program in rodent and human cardiomyocytes.

doi: 10.1038/s41598-018-28239-7

Figure Lengend Snippet: Figure 6. ETV1-transduced neonatal rat ventricular myocytes (NRVMs) upregulates a His-Purkinje system gene signature. (A) Volcano plot of relative transcript expression from NRVMs transduced with either Ad-Etv1- EGFP or Ad-EGFP. RNA-sequencing (RNA-seq) comparison revealed a total of 9,236 differentially expressed genes (normalized counts ≥ 5, padj < 0.05). All significantly different genes (padj < 0.05) are labeled blue (downregulated) or red (enriched) and all nonsignificantly different transcripts labeled in gray. Of these there were 4,696 upregulated and 4,540 downregulated genes in Ad-Etv1-EGFP versus Ad-EGFP transduced NRVMs. (B) Functional clustering of upregulated genes in Ad-Etv1 transduced NRVMs highlighted significantly enriched ETV1-dependent cellular processes (top 20 non-redundant categories are shown). Pathways are color coded to represent genes clustered into functional classes for heat maps in C. (C) Comparative RNA-seq between 21-day-old (P21) wild-type mouse FACS-purified Purkinje cell (PC)/ventricular myocytes (VM) and Ad-Etv1-EGFP/Ad-EGFP transduced NRVMs. Heat map representation of 88 genes differentially expressed in Ad-Etv1-EGFP versus Ad-EGFP transduced NRVMs (n = 3) plotted adjacent to average fold change expression in PCs and VMs. Genes clustered into functional groups demonstrate that ETV1 regulates a PC transcriptome in neonatal cardiomyocytes.

Article Snippet: P1 NRVM heart lysates were purified using Miltenyi Biotec rat neonatal cardiomyocyte isolation kit (Miltenyi Biotec, 130–105–420) according to the manufacture’s protocol.

Techniques: Expressing, Transduction, RNA Sequencing, Comparison, Labeling, Functional Assay, Purification

Journal: Scientific reports

Article Title: ETV1 activates a rapid conduction transcriptional program in rodent and human cardiomyocytes.

doi: 10.1038/s41598-018-28239-7

Figure Lengend Snippet: Figure 8. Activation of ETV1 in human induced pluripotent stem cells-derived cardiomyocytes (hiPSC-CMs) leads to increased expression of rapid conduction genes and sodium current. (A) Schematic representation of hiPSC-CM generation and maturation (day 0–21), transduction of Ad-Etv1-EGFP or Ad-EGFP (day 24), and timepoint for experimentation (day 38–40). (B) Quantitative RT-PCR analysis of Etv1, NKX2–5, GJA5, SCN5A, and MYL2 in hiPSC-CM transduced with either Ad-Etv1-EGFP or Ad-EGFP (n = 4). (C) Whole-cell patch clamp was performed on Ad-Etv1-EGFP (n = 12) or Ad-EGFP (n = 9) transduced hiPSC-CMs. Sodium current–voltage (I–V) relationship comparison. (D) hiPSC-CM NaV peak conductance (gNaV-peak). gNaV-peak following −120 mV to −35 mV depolarization step was measured for Ad-Etv1-EGFP (n = 12) or Ad-EGFP (n = 9) transduced hiPSC-CMs. Data represent mean ± SEM. *P < 0.05, 2-tailed Student’s t test.

Article Snippet: P1 NRVM heart lysates were purified using Miltenyi Biotec rat neonatal cardiomyocyte isolation kit (Miltenyi Biotec, 130–105–420) according to the manufacture’s protocol.

Techniques: Activation Assay, Derivative Assay, Expressing, Transduction, Quantitative RT-PCR, Patch Clamp, Comparison

Journal: Antioxidants (Basel, Switzerland)

Article Title: Intracellular Polyphenol Wine Metabolites Oppose Oxidative Stress and Upregulate Nrf2/ARE Pathway.

doi: 10.3390/antiox11102055

Figure Lengend Snippet: Figure 4. Dose–response effect of wine extract (WE) and sulforaphane (SFN) on oxidative stress- induced intracellular reactive oxygen species (ROS) formation. (a,b) THP-1 cells and cardiomyocytes were pre-incubated with increasing concentrations (from 200 to 800 µg/mL of total polyphenols) of WE and SFN (1–10 µM) before the addition of tert-butyl hydroperoxide (TBHP, 100 µM). Data represent the mean +/−standard deviation of measurements performed in triplicate in three different experiments; * p < 0.01 increase vs. control; ** p < 0.001 decrease vs. THBP; § p < 0.1 decrease vs. TBHP. (c) Representative flow cytometry analysis of ROS generation induced by TBHP and the inhibitory effect of the highest dose of wine extract. (d) Representative flow cytometry analysis on cell viability of the highest dose of wine extract.

Article Snippet: Human cardiomyocyte ventricular primary cells (Celprogen, Torrance, CA, USA) were cultured following the recommended manufacturer’s protocols in extracellular matrix precoated flasks and/or well plates with a ready-to-use complete growth medium (Celprogen, Torrance, CA, USA), as previously described [37].

Techniques: Incubation, Standard Deviation, Control, Cytometry

Journal: Antioxidants (Basel, Switzerland)

Article Title: Intracellular Polyphenol Wine Metabolites Oppose Oxidative Stress and Upregulate Nrf2/ARE Pathway.

doi: 10.3390/antiox11102055

Figure Lengend Snippet: Figure 5. Wine metabolites activate Nrf2/ARE pathway in basal conditions and in cells exposed to oxidative stress. (a,b) Effect of wine extract (WE) and sulforaphane (SFN) on Nrf2 nuclear translocation. THP-1 cells and cardiomyocytes were pre-incubated with WE, containing 800 µg/mL of total polyphenols and 10 µM SFN with or without the addition of tert-butyl hydroperoxide (TBHP, 100 µM). (c) Effect of WE on mRNA expression of Nrf2 target genes hemeoxygenase-1 (HO-1) and glutamate-cysteine ligase catalytic subunit (GCLC). (d) Average quantification of HO-1 and GCLC protein expression obtained by densitometric analysis and representative Western blot analyses for HO-1 and GCLC protein expression in cardiomyocytes. Data represent the mean +/−standard deviation of measurements performed in triplicate in three different experiments and; * p < 0.01 decrease vs. control; § p < 0.01 increase vs. control; ** p < 0.01 vs. TBHP.

Article Snippet: Human cardiomyocyte ventricular primary cells (Celprogen, Torrance, CA, USA) were cultured following the recommended manufacturer’s protocols in extracellular matrix precoated flasks and/or well plates with a ready-to-use complete growth medium (Celprogen, Torrance, CA, USA), as previously described [37].

Techniques: Translocation Assay, Incubation, Expressing, Western Blot, Standard Deviation, Control

Journal: Frontiers in Pharmacology

Article Title: Oleoylethanolamide as a New Therapeutic Strategy to Alleviate Doxorubicin-Induced Cardiotoxicity

doi: 10.3389/fphar.2022.863322

Figure Lengend Snippet: OEA inhibited DOX-induced oxidative stress and apoptosis in cardiomyocytes through TRPV1 pathway. HL-1 cells were treated with 0.1% DMSO, OEA (30 μM), GW6471 (5 μM), capsazepine (10 μM), nonivamide (10 μM), fenofibrate (100 μM) for 30 min. Cells were then treated with DOX (2 μM) for 24 h. Levels of (A) GST (B) TBARS and (C) cell viability was assessed in HL-1 cardiomyocytes. (D) TUNEL positive cells shown in (E) were counted. (E) TUNEL staining of HL-1 cardiomyocytes. Data are expressed as mean ± SEM, n = 4. ***, p < 0.001 vs. control. ##, p < 0.01; ###, p < 0.001 vs. DOX + vehicle. $$$, p < 0.001 vs. DOX + OEA.

Article Snippet: Adult derived primary human cardiomyocytes (Celprogen, Cat # 36044-15) were cultured in complete growth media (Celprogen, Cat #M36044-15S) in an incubator at 37°C with 5% CO 2 atmosphere.

Techniques: TUNEL Assay, Staining, Control

Journal: Frontiers in Pharmacology

Article Title: Oleoylethanolamide as a New Therapeutic Strategy to Alleviate Doxorubicin-Induced Cardiotoxicity

doi: 10.3389/fphar.2022.863322

Figure Lengend Snippet: OEA promotes TRPV1-mediated PI3K/ Akt signaling in cardiomyocytes. HL-1 cells were treated with 0.1% DMSO, OEA (30 μM), GW6471 (5 μM), capsazepine (10 μM) and nonivamide (10 μM) for 30 min. Cells were then treated with DOX (2 μM) for 24 h. PI3K, Akt, p-PI3K and p-Akt was determined using western blot analysis.

Article Snippet: Adult derived primary human cardiomyocytes (Celprogen, Cat # 36044-15) were cultured in complete growth media (Celprogen, Cat #M36044-15S) in an incubator at 37°C with 5% CO 2 atmosphere.

Techniques: Western Blot

Journal: Frontiers in Pharmacology

Article Title: Oleoylethanolamide as a New Therapeutic Strategy to Alleviate Doxorubicin-Induced Cardiotoxicity

doi: 10.3389/fphar.2022.863322

Figure Lengend Snippet: Inhibition of the PI3K-Akt signaling blocks the protective effects of OEA in cardiomyocytes. HL-1 cells were treated with 0.1% DMSO, OEA (30 μM) and LY294002 (10 μM) for 30 min. Cells were then treated with DOX (2 μM) for 24 h. Levels of (A) GST (B) TBARS and (C) cell viability was assessed in HL-1 cardiomyocytes. (D) TUNEL positive cells shown in (F) were counted. (E) Fluorescence quantification for caspase three in (G) were calculated. (F) TUNEL staining of HL-1 cardiomyocytes. (G) Immunofluorescence staining of caspase three in HL-1 cardiomyocytes. Data are expressed as mean ± SEM, n = 4. ***, p < 0.001 vs. control. #, p < 0.05; ##, p < 0.01; ###, p < 0.001 vs. DOX + vehicle. $, p < 0.05; $$, p < 0.01; $$$, p < 0.001 vs. DOX + OEA.

Article Snippet: Adult derived primary human cardiomyocytes (Celprogen, Cat # 36044-15) were cultured in complete growth media (Celprogen, Cat #M36044-15S) in an incubator at 37°C with 5% CO 2 atmosphere.

Techniques: Inhibition, TUNEL Assay, Fluorescence, Staining, Immunofluorescence, Control

Journal: Scientific reports

Article Title: Unlocking cardiac motion: assessing software and machine learning for single-cell and cardioid kinematic insights.

doi: 10.1038/s41598-024-52081-9

Figure Lengend Snippet: Figure 2. Comparison of the three open-source software programs with in-silico cardiomyocytes with 200% time-to-peak. (a) The first experiment with “grey” patterned cardiomyocyte. The plot on the left side of the panel represents the speed profile evaluated by the three software programs. The grey profile is the benchmark considered in this study (MUSCLEMOTION), the cyan profile derives from CONTRACTIONWAVE evaluation, and the orange profile is the ViKiE estimation. The histograms on the right side represent the four parameters extracted by the profiles and measured by the three methodologies. (b) The second experiment with “fog” patterned cardiomyocyte. As in panel (a), the profiles and histograms of the software evaluations are reported to address the ground-truth comparison.

Article Snippet: On the 26th day of culture, the cells were purified from all non-cardiomyocytes by MACS PSC-Derived Cardiomyocyte Isolation Kit (Miltenyi Biotec, #130-110-188) as the negative fraction to depletion antibodies.

Techniques: Comparison, Software, In Silico

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: International Journal of Nanomedicine

Article Title: Mechanisms of greater cardiomyocyte functions on conductive nanoengineered composites for cardiovascular application

doi: 10.2147/IJN.S34574

Figure Lengend Snippet: Addition of CNF to the PLGA substrate alters the topography of the material. Using an Asylum MFP three-dimensional atomic force microscope (scan rate 1.0 Hz, AC mode with 256 × 256 scan points and lines), ( A ) CNF are shown for a 25:75 ratio (PLGA:CNF [wt%:wt%]) sample with a PLGA density of 0.025 g/mL which increases surface nanometer features as well as the total substrate surface area as compared with an etched glass cover slip. ( B ) It is shown for all PLGA:CNF ratio samples that increasing the CNF weight ratio increased the surface area of the substrate by creating nano, submicron, and micron features. ( C ) By normalizing the protein adsorption OD readings to the lowest reading (ie, for the controlled etched glass coverslip) and comparing it with the surface area percent increase, the results indicate that protein saturation was around 40%–55% of amount of increase of the surface area, and provide evidence that increasing the surface area (through addition of CNF) allows more proteins to attach to the surface to promote cell attachment. ( D ) Calculating the normalized protein adsorption capacity indicates that the 75:25 and 50:50 ratios (PLGA:CNF [wt%:wt%]) had the highest ability to attach the most proteins to a particular surface, indicating that one of the mechanisms regulating cardiomyocyte interactions is increasing material protein capacity through altering topographical features by addition of CNF. Notes: This is evident in the similar cardiomyocyte growth trends reported by Stout et al. * P < 0.05 CNF wt% in materials versus 0% CNF wt% in materials; ** P < 0.05 CNF wt% in materials versus 75% CNF wt% in materials; *** P < 0.05 CNF wt% in materials versus 50% CNF wt% in materials; **** P < 0.05 CNF wt% in materials versus 75% CNF wt% in materials, and ***** P < 0.05 CNF wt% in materials versus 100% CNF wt% in materials. Data are shown as the mean count of n = 3. Abbreviations: CNF, carbon nanofibers; OD, optical density; PLGA, poly(lactic-co-glycolic-acid).

Article Snippet: Cells were seeded into 12-well human cardiomyocyte stem cell culture extracellular matrix plates (Celprogen on top of the various PLGA:CNF samples) and 22 mm microscope cover slips (Fisher Science circles No 1, 0.13–0.17 mm thick; size 22 mm) as controls.

Techniques: Microscopy, Adsorption, Cell Attachment Assay

Journal: International Journal of Nanomedicine

Article Title: Mechanisms of greater cardiomyocyte functions on conductive nanoengineered composites for cardiovascular application

doi: 10.2147/IJN.S34574

Figure Lengend Snippet: Cardiomyocyte cell proliferation on a PLGA density of 0.025 g/mL after ( A ) 24, ( B ) 72, and ( C ) 120 hours on 100 nm diameter PLGA:CNF composite materials of interest in this study. Notes: Seeding density was 5 × 104 cells/cm 2 . Data are shown as the mean count of n = 3. The control was the glass substrate. * P < 0.05 versus control; ** P < 0.05 versus similar PLGA:CNF composite ratios and different densities; *** P < 0.05 versus similar PLGA:CNF composite ratios between 24 and 72 hours, and **** P < 0.05 versus PLGA:CNF composite ratios between 72 and 120 hours. Abbreviations: CNF, carbon nanofibers; PLGA, poly(lactic-co-glycolic-acid).

Article Snippet: Cells were seeded into 12-well human cardiomyocyte stem cell culture extracellular matrix plates (Celprogen on top of the various PLGA:CNF samples) and 22 mm microscope cover slips (Fisher Science circles No 1, 0.13–0.17 mm thick; size 22 mm) as controls.

Techniques: Control

Journal: International Journal of Nanomedicine

Article Title: Mechanisms of greater cardiomyocyte functions on conductive nanoengineered composites for cardiovascular application

doi: 10.2147/IJN.S34574

Figure Lengend Snippet: Immunofluorescence staining for cardiomyocyte biomarkers on a 0.025 g/mL PLGA density PLGA:CNF composite after 120 hours of incubation. ( A ) Cardiac troponin T (green) biomarker with DAPI stain (blue) on a 50:50 (PLGA:CNF [wt%:wt%]) sample. ( B ) Connexin-43 (red) with DAPI stain (blue) on a 50:50 (PLGA:CNF [wt%:wt%]) sample. ( C ) α-SCA (yellow) with DAPI stain (blue) on a 50:50 (PLGA:CNF [wt%:wt%]) sample within the cardiomyocytes, indicating cardiomyocyte activity on the materials. Seeding density was 5.5 × 10 4 cells/mL. Scale bar 200 μm. Area fraction (%), area of stain on the surface compared with the total area of image, of DAPI (nucleus) and ( B ) cardiac troponin T, ( D ) connexin-43, and ( F ) α-SCA after 120 hours of cell incubation, on all PLGA:CNF (wt%:wt%) ratio samples. Notes: The results indicate trends similar to those of the adhesion and proliferation experiments , thus verifying those results and indicating cardiomyocyte activity on the materials. Seeding density was 5.5 × 10 4 cells/mL. Data are shown as the mean count of n = 3. Control was glass substrate. * P < 0.05 versus 100:0 (PLGA:CNF [wt%:wt%]) ratio sample; ** P < 0.05 versus 75:25 (PLGA:CNF [wt%:wt%]) ratio sample; *** P < 0.05 versus 50:50 (PLGA:CNF [wt%:wt%]) ratio sample; **** P < 0.05 versus 25:75 (PLGA:CNF [wt%:wt%]) ratio sample; ***** P < 0.05 versus 0:100 (PLGA:CNF [wt%:wt%]) ratio sample, and ****** P < 0.05 versus control sample. Abbreviations: CNF, carbon nanofibers; cTNT, cardiac Troponin-T; PLGA, poly(lactic-co-glycolic-acid).

Article Snippet: Cells were seeded into 12-well human cardiomyocyte stem cell culture extracellular matrix plates (Celprogen on top of the various PLGA:CNF samples) and 22 mm microscope cover slips (Fisher Science circles No 1, 0.13–0.17 mm thick; size 22 mm) as controls.

Techniques: Immunofluorescence, Staining, Incubation, Biomarker Discovery, Activity Assay, Control

Journal: International Journal of Nanomedicine

Article Title: Mechanisms of greater cardiomyocyte functions on conductive nanoengineered composites for cardiovascular application

doi: 10.2147/IJN.S34574

Figure Lengend Snippet: Schematic illustration, with a three-dimensional atomic force microscopy topographical image (scan rate 1.0 Hz, AC mode with a 256 × 256 scan points and lines), of the proposed mechanism by which PLGA:CNF materials may be superior to conventional materials for cardiovascular application. The bioactive surfaces of PLGA:CNF mimic those of the natural myocardium (in stiffness) and increasing protein adsorption capacitance to promote greater amounts of protein adsorption ( A ) and efficiently stimulate cardiomyocyte growth better than conventional materials and plain nanorough surfaces ( B and C ). ( A ) Once a patch is placed into its host, protein adsorption begins on substrates immediately. ( B ) Cardiomyocyte attachment and growths begins. ( C ) Due to mimicking the native myocardium (in stiffness) and ability to increase protein adsorption capacitance, more cardiomyocytes adhere and grow on nanorough stiff material as compared with conventional and plain nanorough materials. Abbreviations: CNF, carbon nanofibers; PLGA, poly(lactic-co-glycolic-acid).

Article Snippet: Cells were seeded into 12-well human cardiomyocyte stem cell culture extracellular matrix plates (Celprogen on top of the various PLGA:CNF samples) and 22 mm microscope cover slips (Fisher Science circles No 1, 0.13–0.17 mm thick; size 22 mm) as controls.

Techniques: Microscopy, Adsorption