STEMdiff™ Ventricular Cardiomyocyte Differentiation Kit
Serum-free media for differentiation of human PSCs to ventricular cardiomyocytes and long-term maintenance of human PSC-derived cardiomyocytes
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Products for Your Protocol
To see all required products for your protocol, please consult the
Protocols and Documentation.
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Gentle Cell Dissociation ReagentcGMP, enzyme-free cell dissociation reagent
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D-PBS (Without Ca++ and Mg++)Dulbecco’s phosphate-buffered saline without calcium and magnesium
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Y-27632 (Dihydrochloride)RHO/ROCK pathway inhibitor; Inhibits ROCK1 and ROCK2
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Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Applications
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Resources and Publications
Educational Materials (15)
Publications (16)
Gremlin1 repression-mediated mitochondrial network hyperfunction contributes to TCE-induced zebrafish cardiac defects
Cell Communication and Signaling : CCS 2025 Jul
Abstract
BackgroundTrichloroethylene (TCE) is a ubiquitous pollutant with potential capacity to induce congenital heart disease (CHD). However, the mechanisms underlying TCE-induced CHD are largely unraveled.MethodsWe exposed zebrafish embryos to TCE to investigate its cardiac development toxicity and related response factor through bulk RNA sequencing. We constructed transgenic fluorescent fish and employed the CRISPR/dCas9 system along with single-cell RNA sequencing to identify the genetic cause of TCE-induced CHD.ResultsWe found that early-stage exposure to TCE induced significant cardiac defects characterized by elongated SV-BA distance, thinned myocardium, and attenuated contractility. Gremlin1 encoding gene, grem1a, a putative target showing high expression at the beginning of cardiac development, was sharply down-regulated by TCE. Consistently, grem1a knockdown in zebrafish induced cardiac phenotypes generally like those of the TCE-treated group, accompanying the disarrangement of myofibril structure. Single-cell RNA-seq depicted that mitochondrial respiration in grem1a-repressed cardiomyocytes was greatly enhanced, ultimately leading to a branch from the normal trajectory of myocardial development. Accordingly, in vitro results demonstrated that GREM1 repression increased mitochondrial content, ATP production, mitochondrial reactive oxygen species, mitochondrial membrane potential, and disrupted myofibril expansion in hPSC-CMs.ConclusionsThese results suggested that TCE-induced gremlin1 repression could result in mitochondrial hyperfunction, thereby hampering cardiomyocyte development and causing cardiac defects in zebrafish embryos. This study not only provided a novel insight into the etiology for environmental stressor-caused cardiac development defects, but also offered a potential therapeutic and preventive target for TCE-induced CHD.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12964-025-02314-9.
Monkeypox virus protein H3L induces injuries in human and mouse
Cell Death & Disease 2024 Aug
Abstract
Monkeypox virus (MPV) is known to inflict injuries and, in some cases, lead to fatalities in humans. However, the underlying mechanisms responsible for its pathogenicity remain poorly understood. We investigated functions of MPV core proteins, H3L, A35R, A29L, and I1L, and discovered that H3L induced transcriptional perturbations and injuries. We substantiated that H3L upregulated IL1A expression. IL1A, in consequence, caused cellular injuries, and this detrimental effect was mitigated when countered with IL1A blockage. We also observed that H3L significantly perturbed the transcriptions of genes in cardiac system. Mechanistically, H3L occupied the promoters of genes governing cellular injury, leading to alterations in the binding patterns of H3K27me3 and H3K4me3 histone marks, ultimately resulting in expression perturbations. In vivo and in vitro models confirmed that H3L induced transcriptional disturbances and cardiac dysfunction, which were ameliorated when IL1A was blocked or repressed. Our study provides valuable insights into comprehensive understanding of MPV pathogenicity, highlights the significant roles of H3L in inducing injuries, and potentially paves the way for the development of therapeutic strategies targeting IL1A.
Role of Blood Oxygen Saturation During Post-Natal Human Cardiomyocyte Cell Cycle Activities.
JACC. Basic to translational science 2020 may
Abstract
Blood oxygen saturation (SaO2) is one of the most important environmental factors in clinical heart protection. This study used human heart samples and human induced pluripotent stem cell-cardiomyocytes (iPSC-CMs) to assess how SaO2 affects human CM cell cycle activities. The results showed that there were significantly more cell cycle markers in the moderate hypoxia group (SaO2: 75{\%} to 85{\%}) than in the other 2 groups (SaO2 {\textless}75{\%} or {\textgreater}85{\%}). In iPSC-CMs 15{\%} and 10{\%} oxygen (O2) treatment increased cell cycle markers, whereas 5{\%} and rapid change of O2 decreased the markers. Moderate hypoxia is beneficial to the cell cycle activities of post-natal human CMs.
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Need a high-quality cell source? Choose from our hiPSC healthy control lines, manufactured with mTeSR™ Plus.
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PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT ƽ, REFER TO WWW.ƽ.COM/COMPLIANCE.
