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1,052 results for “cardiomyocytes”
Single-cell transcriptomic profiling unveils dysregulation of cardiac progenitor cells and cardiomyocytes in a mouse model of maternal hyperglycemia
<p>Congenital heart disease (CHD) is the most prevalent structural malformations of the heart affecting ∼1% of live births. To date, both damaging genetic variations and adverse environmental exposure such as maternal diabetes have been found to cause CHD. Clinical studies show ∼fivefold higher risk of CHD in the offspring of mothers with pregestational diabetes. Maternal pregestational diabetes affects the gene regulatory networks key to proper cardiac development in the fetus. However, the cell-type specificity of these gene regulatory responses to maternal diabetes and their association with the observed cardiac defects in the fetuses remains unknown. To uncover the transcriptional responses to maternal diabetes in the early embryonic heart, we used an established murine model of pregestational diabetes. In this model, we have previously demonstrated an increased incidence of CHD. Here, we show maternal hyperglycemia (matHG) elicits diverse cellular responses during heart development by single-cell RNA-sequencing in embryonic hearts exposed to control and matHG environment. Through differential gene-expression and pseudotime trajectory analyses of this data, we identified changes in lineage specifying transcription factors, predominantly affecting Isl1+ second heart field progenitors and Tnnt2+cardiomyocytes with matHG. Using in vivo cell-lineage tracing studies, we confirmed that matHG exposure leads to impaired second heart field-derived cardiomyocyte differentiation. Finally, this work identifies matHG-mediated transcriptional determinants in cardiac cell lineages elevate CHD risk and show perturbations in Isl1-dependent gene-regulatory network (Isl1-GRN) affect cardiomyocyte differentiation. Functional analysis of this GRN in cardiac progenitor cells will provide further mechanistic insights into matHG-induced severity of CHD associated with diabetic pregnancies.</p>
2D LSFM timelapse of cardiomyocyte calcium dynamics
<p>Uploaded zip-folder contains the following files:<br> 1. A representative raw dataset of a 2D LSFM ventricular cardiomyocyte undergoing stimulated calcium transients and calcium sparks (frame_0000.tif -frame_17999.tif)<br> 2. The recorded pacing signal time trace (waveform_test.xslx)<br> 3. Image corresponding to the time-averaged background (AVG_19_35_39_LowNA rolling shutter.tif)<br> 4. Pre-processed nuclear mask matrix (NuclearMask.mat), CMO-channel average (CMO_Average.mat), and CMO channel maximum intensity projection (CMO_MIP). <br> 5. Split and co-registered data for each spectral channel (CMO_frame_00001.tif-CMO_frame_18000.tif, FLUO4_frame_00001.tif -FLUO4_frame_18000.tif).<br> <br> Compressed file size: 14.9 GB<br> Uncompressed file size: 42.8 GB. <br> <br> Related to the following manuscript: <br> Liuba Dvinskikh, Hugh Sparks, Ken MacLeod and Chris Dunsby " <em>High-speed 2D light-sheet fluorescence microscopy enables quantification of spatially varying calcium dynamics in ventricular cardiomyocytes</em>" (2023), <em>In review</em> with Frontiers in Physiology, Cardiac Electrophysiology. </p>
Pacing of primary murine cardiomyocytes expressing human TRPV1 using infra-red laser
<h2>Abstract</h2> <p>The expression of human TRPV1 in cardiomyocytes allowed us to induce action potentials (APs) by pulse irradiation with infra-red (IR) diod laser. Mice cardiomyocytes were transformed by AAV-based vectors bearing construction of TRPV1 with mRuby (for expression detection). We selected cells having their own intrisic AP generation and then set them up for measuring membrane potential in a current-clamp mode. Cells were irradiated using 2 or 7 Hz laser pulses. Laser trigger pulses were recorded along with cell potential. In the dataset <em><strong>05-12-22.zip</strong></em>, there are some records where electrical stimulation were used alone or together with IR pulses. Experimental conditions are summarized in the file <em><strong>experiment-descriptions.tsv</strong></em>.</p> <h2>Primary cell production and transformation</h2> <p>Experiments were carried out using C57Bl/6J mice (The Jackson Laboratory, #000664, RRID: IMSR_JAX:000664). The mixed mouse primary neonatal cardiomyocyte cell culture was obtained using a neonatal heart dissociation kit (Miltenyi Biotec, 130-098-373) according to the manufacturer’s instructions. The cells were cultured in DMEM/F12, 1:1 mixture (BioloT, 1.3.7.2.) supplemented with 10% FBS, penicillin 100 U/ml /streptomycin 100 mg/ml, and L-glutamine 0.365 g/l. The culture was seeded on 10mm coverslips coated with 10 mg/ml gelatin diluted in PBS and maintained at 37℃ in 5% CO2. For transient expression of the hTRPV1 channel, a reporter protein, and a fluorescent Ca2+ sensor GCaMP6s, we used AAV-based vectors with the encoded genes above. We used AAV-DJ serotype at a MOI of 12,000 VG/cells for cTnT_hTRPV1(sh)_P2A_mRuby based viruses, and a MOI of 2,500 VG/cells for cTnT_GCaMP6s ones. The cells were infected on the next day after plating, and the transgene expression peak was observed on the third day after the infection.</p> <h2>Distant heating system</h2> <p>The system was equipped with a fiber coupled laser diode (LD) 4PN-117 (SemiNex) as a powerful heating laser, providing radiation at a wavelength of 1375 nm with an average power of up to 4.3 W through a multimode fiber with a core diameter of 105 μm and 0.22NA. The LD was mounted onto a TEC-controlled plate “264 TEC HP LaserMount” (A.I.), which was operated by TEC driver TECSource 5305 (A.I.); current stabilization and control for LD were performed with LD driver LaserSource 4320 (A.I.). The laser was controlled via the TTL output from the HEKA EPC-10 amplifier. Different laser intensities, and pulse widths were used. Laser power, <em><strong>P</strong></em>, can be computed from trigger voltage, <em><strong>U</strong></em>, by an equation: <em><strong>P [W] = -0.28 + 1.42 * U [V]</strong></em></p> <h2>Electrophysiology of single cardiac cells </h2> <p>Patch electrodes were pulled from hard borosilicate capillary glass (Sutter Instruments flaming/brown micropipette puller) and filled with an intracellular solution consisting of (in mM) K-gluconate, 100; KCl, 40; HEPES, 10; NaCl, 8; MgATP, 4; MgGTP, 0.3; phosphocreatine, 10 (pH 7.3 with KOH). Cells were identified visually using IR-video microscopy using a Hamamatsu ORCA-Flash4.0 V3 Digital sCMOS camera (Hamamatsu Photonics) expression of wild type or mutant TRPV1 was confirmed by the presence of red flourescent protein. Coverslips were placed in a recording chamber continuously perfused with heated Tyrode's solution. Whole-cell recordings were taken at 32°C in current-clamp mode using a HEKA EPC-10 amplifier (List Elektronik) with a sampling rate of 100 μs. Steady state current was injected to achieve a membrane potential of approximately −60 to −90 mV. For experiments using the IR laser the optic fiber was placed near the cell, and light from a green laser diode was shone onto the cell to check correct positioning. </p>
Electrophysiological recordings from human-derived cardiomyocytes in the form of MEA (microelectrode array) recordings
<p><span>The electrophysiological data were acquired using standard software for MEA acquisition, such as the programs provided with the used MEA acquisition system coupled with the SiMulTox prototype.</span></p>
Supplementary videos for the "Remote-refocusing light-sheet fluorescence microscopy enables 3D imaging of electromechanical coupling of hiPSC-derived and adult cardiomyocytes in co-culture" manuscript
<p>Supplementary videos for preprint manuscript: </p> <p><em>Remote-refocusing light-sheet fluorescence microscopy enables 3D imaging of electromechanical coupling of hiPSC-derived and adult cardiomyocytes in co-culture</em><br> Liuba Dvinskikh, Hugh Sparks, Liliana Brito, Kenneth T MacLeod, Sian E Harding, Christopher Dunsby<br> bioRxiv 2023.01.28.526043; doi: https://doi.org/10.1101/2023.01.28.526043</p> <p>All videos have been rendered with JPEG compression.</p> <p>Shortened video captions (Please see supplementary information document for full caption)<br> <strong>Video 1:</strong> 3D LSFM timelapse of hiPSC-CM undergoing spontaneous calcium transients. <br> <strong>Video 2:</strong> Widefield transillumination timelapse of hiPSC-CM and adult-CM <br> <strong>Video 3:</strong> Widefield fluorescence timelapse of hiPSC-CM and adult CM with synchronized spontaneous calcium transients. <br> <strong>Video 4a:</strong> 3D LSFM timelapse of hiPSC-CM and adult-CM day 1 co-culture undergoing synchronized spontaneous transients. <br> <strong>Video 4b</strong>: Depth-encoded MIPs of the 3D LSFM timelapse of hiPSC-CM and adult-CM day 1 co-culture undergoing synchronized spontaneous transients. <br> <strong>Video 5a:</strong> 3D LSFM timelapse of hiPSC-CM and adult-CM day 1 co-culture undergoing synchronized spontaneous transients in a sample without NBleb. <br> <strong>Video 5b</strong>: Depth-encoded MIPs of the 3D LSFM timelapse of hiPSC-CM and adult-CM day 1 co-culture without NBleb undergoing synchronized spontaneous transients. <br> <strong>Video 6a</strong>: 3D LSFM timelapse of hiPSC-CM and adult-CM co-culture undergoing synchronized spontaneous transients in a sample treated with NBleb. <br> <strong>Video 6b:</strong> Depth-encoded MIPs of the 3D LSFM timelapse of hiPSC-CM and adult-CM day 1 co-culture with NBleb undergoing synchronized spontaneous transients. <br> <strong>Video 7a:</strong> 3D LSFM timelapse of hiPSC-CM and adult-CM day 0 co-culture undergoing synchronized spontaneous transients in a sample without NBleb. <br> <strong>Video 7b: </strong>Depth-encoded MIPs of the 3D LSFM timelapse of hiPSC-CM and adult-CM day 0 co-culture without NBleb. </p> <p> </p>
Computationally-informed point of departure evaluation for proarrhythmic cardiotoxicity assessment using 3D engineered cardiac microtissues from human iPSC-derived cardiomyocytes
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Cardio PyMEA: A user-friendly, open-source Python application for cardiomyocyte microelectrode array analysis
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Vasohibin1, a new mouse cardiomyocyte IRES trans-acting factor that regulates translation in early hypoxia
Hypoxia, a major inducer of angiogenesis, triggers major changes in gene expression at the transcriptional level. Furthermore, under hypoxia, global protein synthesis is blocked while internal ribosome entry sites (IRES) allow specific mRNAs to be translated. Here, we report the transcriptome and translatome signatures of (lymph)angiogenic genes in hypoxic HL-1 mouse cardiomyocytes: most genes are induced at the translatome level, including all IRES-containing mRNAs. Our data reveal activation of (lymph)angiogenic factor mRNA IRESs in early hypoxia. We identify vasohibin1 (VASH1) as an IRES trans-acting factor (ITAF) that is able to bind RNA and to activate the FGF1 IRES in hypoxia, but which tends to inhibit several IRESs in normoxia. VASH1 depletion has a wide impact on the translatome of (lymph)angiogenesis genes, suggesting that this protein can regulate translation positively or negatively in early hypoxia. Translational control thus appears as a pivotal process triggering new vessel formation in ischemic heart.
Induced pluripotent stem cell-derived cardiomyocyte in vitro models: tissue fabrication protocols, assessment methods, and quantitative maturation metrics for benchmarking progress
<p>The advent of human induced pluripotent stem cells (hiPSCs) and techniques to differentiate cardiomyocytes from them has opened a viable path to creating <em>in vitro</em> models of normal and diseased hearts, accelerating more predictive drug screening and therapeutic strategies for cardiac pathologies. Currently, hiPSC-derived cardiomyocytes (hiPSC-CMs) are more similar to fetal than adult cardiomyocytes, leading many in the field to explore approaches to enhance cell and tissue maturation. There are over 2,000 studies utilizing hiPSC-CMs in models composed of various combinations of cell and extracellular matrix components, using a plethora of differentiation protocols, culture formats, and methods for quantifying cardiomyocyte function. To assess the current state of this rapidly growing area, we systematically analyzed 300 studies using hiPSC-CM models for their selection of hiPSC lines, hiPSC-CM differentiation protocols, types of <em>in vitro </em>models, maturation techniques, and metrics used to assess cardiomyocyte functionality and maturity. Here, we provide the data compiled from our analysis of these papers so others in the field can utilize it to inform their research.</p> <p>Based on this analysis, we highlight the diversity of, and current trends in, <em>in vitro</em> model designs and highlight the most common and promising practices for functional assessments. We further analyzed outputs spanning structural maturity, contractile function, electrophysiology, and gene expression and note field-wide improvements over time. Finally, we observe that a persistent lack of coordination amongst investigators is limiting the field's ability to benchmark and advance hiPSC-CM function against previous studies. We discuss opportunities to collectively pursue the common goal of hiPSC-CM model development, maturation, and assessment that we believe are critical to drive the entire community forward in engineering mature cardiac tissue.</p>
Increased Drp1 acetylation by lipid overload induces cardiomyocyte death and heart dysfunction
<p>Metabolic syndrome is a cluster of abnormalities characterized by obesity and insulin resistance, which compromise energy metabolism, damage mitochondria, cause cardiomyocyte death, and eventually impair heart contraction and relaxation performance. Despite the increasing prevalence of heart complications in obese and diabetic patients, our knowledge on how obese and diabetes mellitus impair heart function is very limited. In this study, we used animal and cell culture models in rodents or monkeys and generated lipid overload models to mimic obesity conditions. We found that excessive lipid supply decreased nicotinamide adenine dinucleotide (oxidized) levels and increased the acetylation of a fission protein Drp1 at a specific lysine residue (K642). Drp1 acetylation at K642 activated Drp1 through phosphorylation, mitochondrial translocation, and oligomerization. The excessively activated Drp1 had higher GTPase activity, bound with VDAC1 on mitochondria, induced mitochondrial fission, and caused cardiomyocyte death. These findings provide new information regarding how lipid overload regulates redox environment, protein acetylation, and the function of mitochondrial fission protein Drp1 in the heart.</p>
Calcium dynamics upon heating in murine neonatal cardiomyocytes transduced with truncated human TRPV1(−109 a.a.) and the localization of TRPV1 in these cells
<h3>Abstract</h3> <p>The expression of truncated human TRPV1(−109 a.a.) in cardiomyocytes allowed us to induce action potentials (APs) by pulse irradiation with an infrared (IR) diode laser. We studied the calcium dynamics in these cells (Ca_TRPV.zip image set). Murine cardiomyocytes were transducted by AAV-based vectors bearing construction of TRPV1(−109 a.a.) with mRuby (for expression detection) and vectors bearing GCaMP6s calcium sensor. Cardiomyocytes were heated by IR laser with a repetition rate of 2 Hz and 30 ms pulse width in a calcium-free medium.<br>To explain the observed calcium dynamics, we also studied the subcellular localization of human TRPV1 in Murine cardiomyocytes ER_a-flag_100x_param1_Z-stack002.nd2</p> <h3>Primary cell production and transformation</h3> <p>Experiments were carried out using C57Bl/6J mice (The Jackson Laboratory, #000664, RRID: IMSR_JAX:000664). The mixed mouse primary neonatal cardiomyocyte cell culture was obtained using a neonatal heart dissociation kit (Miltenyi Biotec, 130-098-373) according to the manufacturer’s instructions. The cells were cultured in DMEM/F12, 1:1 mixture (BioloT, 1.3.7.2.) supplemented with 10% FBS, penicillin 100 U/ml /streptomycin 100 mg/ml, and L-glutamine 0.365 g/l. The culture was seeded on 10mm coverslips coated with 10 mg/ml gelatin diluted in PBS and maintained at 37℃ in 5% CO2. For transient expression of the hTRPV1 channel, a reporter protein, and a fluorescent Ca2+ sensor GCaMP6s, we used AAV-based vectors with the encoded genes above. We used the AAV-DJ serotype at a MOI of 12,000 VG/cells for cTnT_hTRPV1(sh)_P2A_mRuby based viruses, and a MOI of 2,500 VG/cells for cTnT_GCaMP6s ones. The cells were infected on the next day after plating, and the transgene expression peak was observed on the third day after the infection.</p> <h3>Distant heating system</h3> <p>The system was equipped with a fiber coupled laser diode (LD) 4PN-117 (SemiNex) as a powerful heating laser, providing radiation at a wavelength of 1375 nm with an average power of up to 4.3 W through a multimode fiber with a core diameter of 105 μm and 0.22NA. The LD was mounted onto a TEC-controlled plate “264 TEC HP LaserMount” (A.I.), which was operated by TEC driver TECSource 5305 (A.I.); current stabilization and control for LD were performed with LD driver LaserSource 4320 (A.I.). The laser was controlled via the TTL output from the HEKA EPC-10 amplifier. Different laser intensities and pulse widths were used. Laser power, P, can be computed from trigger voltage, U, by an equation: P [W] = -0.28 + 1.42 * U [V].</p> <p>Intracellular calcium recordings of single cardiac cells<br>Neonatal cardiomyocyte cells transduced with GCaMP6s sensor were viewed and acquired under a water immersion Olympus LUMPLFLN40×W objective with 40X magnification. Data acquisition was performed at 20 fps using a Scientifica SliceScopePro 2000 microscope (Scientifica, UK) equipped with a Hamamatsu Orca Flash 4.0 CMOS monochrome digital camera (Hamamatsu Photonics) connected to a PC running the free software uManager. A CoolLED pE-300ultra was used as a light source. It was synchronized with the laser heating system via BNC-TTL output from the Heka Elektronik EPC 10 USB Patch Clamp Amplifier. To synchronize the pacing and the GCamp6s signal registration, the light source was switched off for one acquisition cycle at the beginning of the pacing. The GCamp6s signal was analyzed using Fiji software.</p> <h3><br>TRPV1 channel localization</h3> <p>To understand the localization of the expressed TRPV1 channels in neonatal mice cardiomyocytes, we utilized cells infected with AAV-PHP.S serotype viruses with pAAV_cTnT_hTRPV1_P2A_FLAG-tag at a MOI of 2500 VG/cells. To visualize endoplasmic reticulum, we stained the live cells with ER-Tracker™ Red (BODIPY™ TR Glibenclamide, Thermo Fisher Scientific, E34250) according to the manufacturer’s instructions. After the staining with ER-tracker, cardiomyocytes were fixed with 4% paraformaldehyde (Sigma-Aldrich, 158127-100G) for 5 minutes at room temperature and washed trice with 0.3% Tween 20 (Sigma-Aldrich, P1379-250ML) diluted in PBS (5 minutes each). The fixed cells then were blocked with PBS containing 0.12% tween 20, 1% bovine serum albumin (BSA, PanEko, 68100.10г), and 10% goat serum (Thermo Fisher Scientific, 16210072) for 40 minutes at room temperature. After the buffer removal, the cardiomyocytes were labeled with of DYKDDDDK Tag Recombinant Rabbit Monoclonal Antibody (8H8L17, Invitrogen, MA1-142-A488) at 1:500 dilution in 1% BSA, 10% goat serum, and 89% PBS for 2 hours at room temperature. The samples were washed three times with PBS after the incubations. Then, the cells were stained with Goat anti-Rabbit IgG (H+L) Cross-Adsorbed Secondary Antibody Alexa Fluor™ 488 (Invitrogen, A-11008) at dilution 1:500 for 1 hour at room temperature. The removal of non-conjugated antibodies was performed in parallel with cell nuclei staining. The cells were incubated with PBS supplemented with 2 μg/ml DAPI (Miltenyi Biotec, 130-111-570) for 15 minutes at room temperature. For further experiments, glasses with the labeled cells were placed onto the Superfrost Plus adhesion slides (Epredia, EPBRSF41296SP) in 20 µl VECTASHIELD Vibrance Antifade Mounting Media (Vector Laboratories, H-1700-2) and stored at +4℃ in the dark.<br>The samples were analyzed using an inverted Nikon A1 confocal microscope and visualized using Nikon NIS-Elements software. We pictured the sample in each channel individually exciting DAPI, DYKDDDDK Tag-Alexa Fluor 488, and ER-tracker by laser lines 405 nm, 488 nm and 561 nm, respectively. Colocolization analysis was performed using ImageJ software.</p>
Data from: Major group-B enterovirus populations deleted in the noncoding 5' region of genomic RNA modulate activation of the type I interferon pathway in cardiomyocytes and induce myocarditis
<p>Major 5'-terminally deleted (5'TD) RNA forms of group-B coxsackievirus (CVB-5'TD) has been associated with myocarditis in both mice and humans. Although it is known that interferon-β (IFN-β) signaling is critical for an efficient innate immune response against CVB-induced myocarditis, the link between CVB-5'TD RNA forms and type I IFN signaling in cardiomyocytes remains to be explored. In a mouse model of CVB3/28-induced myocarditis, major early-emerging forms of CVB-5'TD RNA have been characterized as replicative viral populations that impair IFN-β production in the heart. Synthetic CVB3/28 RNA forms mimicking each of these major 5'TD virus populations were transfected in mice and have been shown to modulate innate immune responses in the heart and to induce myocarditis in mice. Remarkably, transfection of synthetic viral RNA with deletions in the secondary structures of the 5'-terminal CVB3 RNA domain I, modifying stem-loops "b", "c" or "d", were found to impair IFN-β production in human cardiomyocytes. In addition, the activation of innate immune response by Poly(I:C), was found to restore IFN-β production and to reduce the burden of CVB-5'TD RNA-forms in cardiac tissues, thereby reducing the mortality rate of infected mice. Overall, our results indicate that major early-emerging CVB3 populations deleted in the domain I of genomic RNA, in the 5' noncoding region, modulate the activation of the type I IFN pathway in cardiomyocytes and induce myocarditis in mice. These findings shed new light on the role of replicative CVB-5'TD RNA forms as key pathophysiological factors in CVB-induced human myocarditis.</p>
The mRNA expression changes in neonatal primary mouse ventricular cardiomyocytes treated with epirubicin (2uM)
<p>Epirubicin (EPI) is effective in the treatment of malignant cancers, but its application is limited by life-threatening cardiotoxicity. Iron homeostasis disturbance has been implicated in anthracycline-induced cardiotoxicity (AIC), and ferroptosis is involved in AIC which is dependent upon intracellular iron. However, the role and exact mechanisms of ferroptosis in the pathogenesis of epirubicin-induced cardiotoxicity (EIC) remain elusive. In this study, we aimed to investigate mechanisms underlying ferroptosis-driven EIC. Epirubicin triggered ferroptosis both <em>in vivo</em> and in cultured cardiomyocytes, and pretreatment with ferroptosis inhibitor, Ferrostatin-1(Fer-1) alleviates EIC. Microarray analysis was performed to screen for potential molecules involved in EIC in neonatal primary mouse ventricular cardiomyocytes (NMVMs). We found that the transcript level of ATP6V0A2, a subunit of vacuolar ATPase (V-ATPase), was significantly downregulated when NMVMs were subjected to EPI, which was verified <em>in vivo </em>and <em>in vitro</em> as measured by real-time quantitative reverse transcription PCR (qRT-PCR) and immunoblotting. Intriguingly, overexpression of ATP6V0A2 effectively decreased excessive oxidative stress and lipid-peroxidation accumulation, thereby inhibiting ferroptosis and protecting cardiomyocytes against EIC, as evidenced by functional, enzymatic, and morphological changes. Mechanistically, forced expression of ATP6V0A2 restored lysosomal acidification in EPI-treated cardiomyocytes and protected cardiomyocytes and mice hearts from ferroptosis-driven EIC. In this study, our data elucidate that ferroptosis is involved in EIC, which is ignited by ATP6V0A2-dependent lysosomal acidification dysfunction. Our study provides a new potential therapeutic target for ameliorating EIC.</p>
Fluorescence images acquisition on cultures of human-derived cardiomyocytes
<p><span>These data are used to evaluate the performance of the SiMulTox platform in terms of performance of live-cell fluorescence imaging.</span></p>
CARDIOMYOCYTE RYANODINE RECEPTOR CLUSTERS EXPAND AND COALESCE AFTER APPLICATION OF ISOPROTERENOL
<p>This is data that was used to generate the figures and tables for the Journal of General Physiology paper<br> CARDIOMYOCYTE RYANODINE RECEPTOR CLUSTERS EXPAND AND COALESCE AFTER APPLICATION OF ISOPROTERENOL</p> <p>The data is in two parts: i) Blink data that records the positions of blinks collected from fluorescently labelled ryanodine receptors on the surface of rat ventricular myocytes. ii) Cluster data that records parameters from each of the clusters created by the blink data. </p> <p>The blink data was used to generate Figs. 1 to 4, S3 to S5, while cluster data was used to generate the tables<br> and Figs. 5 to 9. More detailed explanations of the data are in the files blinkinfo.html and clustinfo.html in their respective<br> directories.</p>
Data from: The deubiquitinase USP5 prevents accumulation of protein aggregates in cardiomyocytes
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Electrophysiology data for NAA10-R4S-induced pluripotent-derived cardiomyocytes
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SNTA1-deficient human cardiomyocytes demonstrate hypertrophic phenotype and calcium handling disorder
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Data from: Excitation-contraction coupling, cardiomyocyte electrophysiology, and transcriptome profiles in two HFpEF murine models: Etiology and sex-dependent differences
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Data from: Robotic manipulation of cardiomyocytes to identify gap junction modifiers for arrhythmogenic cardiomyopathy
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
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The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.