Tag Archives: cardiomyocytes

Disease Phenotypes and Mechanisms of iPSC-Derived Cardiomyocytes from Brugada Syndrome Patients with a Loss-of-Function SCN5A Mutation

The authors investigated the pathophysiological phenotypes and mechanisms using induced pluripotent stem cell-derived cardiomyocytes from two Brugada syndrome patients carrying a heterozygous SCN5A mutation p.S1812X.
[Frontiers in Cell and Developmental Biology]
Li, W., Stauske, M., Luo, X., Wagner, S., Vollrath, M., Mehnert, C. S., Schubert, M., Cyganek, L., Chen, S., Hasheminasab, S.-M., Wulf, G., El-Armouche, A., Maier, L. S., Hasenfuss, G., & Guan, K. (2020). Disease Phenotypes and Mechanisms of iPSC-Derived Cardiomyocytes From Brugada Syndrome Patients With a Loss-of-Function SCN5A Mutation. Frontiers in Cell and Developmental Biology, 8. https://doi.org/10.3389/fcell.2020.592893 Cite
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Interaction of the Joining Region in Junctophilin-2 with the L-Type Ca2+ Channel Is Pivotal for Cardiac Dyad Assembly and Intracellular Ca2+ Dynamics

Modified abundance of JPH2 and redistribution of L-type calcium channels were studied in left ventricular hypertrophy in vivo and in cultured adult feline and rat ventricular myocytes.
[Circulation Research]
Gross Polina, Johnson Jaslyn, Romero Carlos M, Eaton Deborah M, Poulet Claire, Sanchez-Alonso Jose L, Lucarelli Carla, Ross Jean, Gibb Andrew A, Garbincius Joanne F, Lambert Jonathan, Varol Erdem, Yang Yijun, Wallner Markus, Feldsott Eric A, Kubo Hajime, Berretta Remus M, Yu Daohai, Rizzo Victor, … Houser Steven R. (n.d.). Interaction of the Joining Region in Junctophilin-2 with the L-type Ca2+ Channel Is Pivotal for Cardiac Dyad Assembly and Intracellular Ca2+ Dynamics. Circulation Research, 0(0). https://doi.org/10.1161/CIRCRESAHA.119.315715 Cite
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BRD4 Interacts with GATA4 to Govern Mitochondrial Homeostasis in Adult Cardiomyocytes

The authors showed that cardiomyocyte-specific deletion of Brd4 in adult mice leads to acute deterioration of cardiac contractile function with mutant animals demonstrating a transcriptomic signature enriched for decreased expression of genes critical for mitochondrial energy production.
[Circulation]
Padmanabhan Arun, Alexanian Michael, Linares-Saldana Ricardo, González-Terán Bárbara, Andreoletti Gaia, Huang Yu, Connolly Andrew J., Kim Wonho, Hsu Austin, Duan Qiming, Winchester Sarah A. B., Felix Franco, Perez-Bermejo Juan A., Wang Qiaohong, Li Li, Shah Parisha P., Haldar Saptarsi M., Jain Rajan, & Srivastava Deepak. (n.d.). BRD4 Interacts with GATA4 to Govern Mitochondrial Homeostasis in Adult Cardiomyocytes. Circulation, 0(0). https://doi.org/10.1161/CIRCULATIONAHA.120.047753 Cite
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Mir-30d Regulates Cardiac Remodeling by Intracellular and Paracrine Signaling

In rat and mouse models of ischemic heart failure, investigators showed that miR-30d gain of function improves cardiac function, decreases myocardial fibrosis, and attenuates cardiomyocyte apoptosis.
[Circulation Research]
Li Jin, Salvador Ane M, Li Guoping, Valkov Nedyalka, Ziegler Olivia, Yeri Ashish Suresh, Xiao Chun Yang, Meechoovet Bessie, Alsop Eric, Rodosthenous Rodosthenis S, Kundu Piyusha, Huan TianXiao, Levy Daniel, Tigges John C, Pico Alexander R, Ghiran Ionita, Silverman Michael G, Meng Xiangmin, Kitchen Robert, … Das Saumya. (n.d.). Mir-30d Regulates Cardiac Remodeling by Intracellular And Paracrine Signaling. Circulation Research, 0(0). https://doi.org/10.1161/CIRCRESAHA.120.317244 Cite
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Comparison of 10 Control hPSC Lines for Drug Screening in an Engineered Heart Tissue Format

Scientists investigated ten different control hiPSC-cardiomyocyte (CM) lines and analyzed function and suitability for drug screening. Five commercial and five academic hPSC-CM lines were casted in engineered heart tissue format.
[Stem Cell Reports]
Mannhardt, I., Saleem, U., Mosqueira, D., Loos, M. F., Ulmer, B. M., Lemoine, M. D., Larsson, C., Améen, C., Korte, T. de, Vlaming, M. L. H., Harris, K., Clements, P., Denning, C., Hansen, A., & Eschenhagen, T. (2020). Comparison of 10 Control hPSC Lines for Drug Screening in an Engineered Heart Tissue Format. Stem Cell Reports, 15(4), 983–998. https://doi.org/10.1016/j.stemcr.2020.09.002 Cite
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Soluble Factors Released by Dedifferentiated Fat Cells Reduce the Functional Activity of iPS Cell‐Derived Cardiomyocytes

Scientists evaluated the effects of soluble factor interactions in indirect cocultures of dedifferentiated fat cells and induced pluripotent stem cell‐derived cardiomyocytes.
[Cell Biology International]
Watanabe, H., Kanemaru, K., Hagikura, K., Matsumoto, T., Ayusawa, M., & Morioka, I. (n.d.). Soluble factors released by dedifferentiated fat cells reduce the functional activity of iPS cell-derived cardiomyocytes. Cell Biology International, n/a(n/a). https://doi.org/10.1002/cbin.11487 Cite
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Redox-Resistant SERCA Attenuates Oxidant-Stimulated Mitochondrial Calcium and Apoptosis in Cardiac Myocytes and Pressure Overload-Induced Myocardial Failure in Mice

Scientists hypothesized that sarco(endo)plasmic reticulum calcium ATPase oxidation at C674 would modulate the effects of reactive oxygen species on mitochondrial calcium and mitochondria-dependent apoptosis in cardiac myocytes.
[Circulation]
Goodman Jena B., Qin Fuzhong, Morgan Robert, Chambers Jordan M., Croteau Dominique, Siwik Deborah A., Hobai Ion, Panagia Marcello, Luptak Ivan, Bachschmid Markus, Tong Xiao Yong, Pimentel David R., Cohen Richard A., & Colucci Wilson S. (n.d.). Redox-Resistant SERCA Attenuates Oxidant-Stimulated Mitochondrial Calcium and Apoptosis in Cardiac Myocytes and Pressure Overload-Induced Myocardial Failure in Mice. Circulation, 0(0). https://doi.org/10.1161/CIRCULATIONAHA.120.048183 Cite
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Nkx2-5 Defines Distinct Scaffold and Recruitment Phases during Formation of the Murine Cardiac Purkinje Fiber Network

Scientists applied genetic fate mapping and temporal clonal analysis to identify murine cardiomyocytes committed to the Purkinje fiber (PF) lineage as early as E7.5. They found that a polyclonal PF network emerged by progressive recruitment of conductive precursors to this scaffold from a pool of bipotent progenitors.
[Nature Communications]
Choquet, C., Kelly, R. G., & Miquerol, L. (2020). Nkx2-5 defines distinct scaffold and recruitment phases during formation of the murine cardiac Purkinje fiber network. Nature Communications, 11(1), 5300. https://doi.org/10.1038/s41467-020-19150-9 Cite
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GATA6 Mutations in hiPSCs Inform Mechanisms for Maldevelopment of the Heart, Pancreas, and Diaphragm

To define molecular mechanisms for the damaging cardiac outflow tract defects caused by GATA6 variants, scientists studied transcriptional and epigenetic responses to GATA6 loss of function and missense variants during cardiomyocyte differentiation of isogenic human iPSCs.
[eLife]
Sharma, A., Wasson, L. K., Willcox, J. A., Morton, S. U., Gorham, J. M., DeLaughter, D. M., Neyazi, M., Schmid, M., Agarwal, R., Jang, M. Y., Toepfer, C. N., Ward, T., Kim, Y., Pereira, A. C., DePalma, S. R., Tai, A., Kim, S., Conner, D., Bernstein, D., … Seidman, C. E. (2020). GATA6 mutations in hiPSCs inform mechanisms for maldevelopment of the heart, pancreas, and diaphragm. ELife, 9, e53278. https://doi.org/10.7554/eLife.53278 Cite
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Progesterone, via Yes-Associated Protein (YAP), Promotes Cardiomyocyte Proliferation and Cardiac Repair

Progesterone supplementation enhanced cardiomyocyte proliferation in a progesterone receptor‐dependent manner. Progesterone up‐regulated YAP expression and knockdown of YAP by small interfering RNA reduced progesterone‐mediated cardiomyocyte proliferative effect.
[Cell Proliferation]
Lan, C., Cao, N., Chen, C., Qu, S., Fan, C., Luo, H., Zeng, A., Yu, C., Xue, Y., Ren, H., Li, L., Wang, H., Jose, P. A., Xu, Z., & Zeng, C. (n.d.). Progesterone, via yes-associated protein, promotes cardiomyocyte proliferation and cardiac repair. Cell Proliferation, n/a(n/a), e12910. https://doi.org/10.1111/cpr.12910 Cite
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Long Non-Coding RNA PVT1 Facilitates High Glucose-Induced Cardiomyocyte Death Through the miR-23a-3p/CASP10 Axis

Investigators observed that plasmacytoma variant translocation 1 (PVT1) and caspase‐10 were upregulated while miR‐23a‐3p was downregulated in high glucose‐induced cardiomyocytes. High glucose repressed cardiomyocyte activity and induced cardiomyocyte apoptosis, but this influence was antagonized by PVT1 knockdown or miR‐23a‐3p overexpression.
[Cell Biology International]
Xia, Y.-W., & Wang, S.-B. (n.d.). Long non-coding RNA PVT1 facilitates high glucose-induced cardiomyocyte death through the miR-23a-3p/CASP10 axis. Cell Biology International, n/a(n/a). https://doi.org/10.1002/cbin.11479 Cite
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