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    Por favor, use este identificador para citar o enlazar este ítem:https://uvadoc.uva.es/handle/10324/64481

    Título
    BIN1 induces the formation of T-tubules and adult-like Ca2+ release units in developing cardiomyocytes
    Autor
    De La Mata Sampedro, AnaAutoridad UVA Orcid
    Tajada Esteban, SendoaAutoridad UVA
    O'Dwyer, Samantha
    Matsumoto, Collin
    Dixon, Rose E.
    Hariharan, Nirmala
    Moreno, Claudia M.
    Santana, Luis Fernando
    Año del Documento
    2019
    Editorial
    Wiley Periodicals
    Descripción
    Producción Científica
    Documento Fuente
    Stem Cells, 2019, vol. 37, n. 1, p. 54-64
    Resumen
    Human embryonic stem cell-derived cardiomyocytes (hESC-CMs) are at the center of new cell-based therapies for cardiac disease, but may also serve as a useful in vitro model for cardiac cell development. An intriguing feature of hESC-CMs is that although they express contractile proteins and have sarcomeres, they do not develop transverse-tubules (T-tubules) with adult-like Ca2+ release units (CRUs). We tested the hypothesis that expression of the protein BIN1 in hESC-CMs promotes T-tubules formation, facilitates CaV 1.2 channel clustering along the tubules, and results in the development of stable CRUs. Using electrophysiology, [Ca2+ ] imaging, and super resolution microscopy, we found that BIN1 expression induced T-tubule development in hESC-CMs, while increasing differentiation toward a more ventricular-like phenotype. Voltage-gated CaV 1.2 channels clustered along the surface sarcolemma and T-tubules of hESC-CM. The length and width of the T-tubules as well as the expression and size of CaV 1.2 clusters grew, as BIN1 expression increased and cells matured. BIN1 expression increased CaV 1.2 channel activity and the probability of coupled gating within channel clusters. Interestingly, BIN1 clusters also served as sites for sarcoplasmic reticulum (SR) anchoring and stabilization. Accordingly, BIN1-expressing cells had more CaV 1.2-ryanodine receptor junctions than control cells. This was associated with larger [Ca2+ ] transients during excitation-contraction coupling. Our data support the view that BIN1 is a key regulator of T-tubule formation and CaV 1.2 channel delivery. By studying the role of BIN1 during the differentiation of hESC-CMs, we show that BIN1 is also important for CaV 1.2 channel clustering, junctional SR organization, and the establishment of excitation-contraction coupling
    Palabras Clave
    hESC
    Cardiac myocytes
    BIN1
    T-tubules
    CaV1.2
    Calcium release units
    ISSN
    1066-5099
    Revisión por pares
    SI
    DOI
    10.1002/stem.2927
    Propietario de los Derechos
    © 2018 The Authors
    Idioma
    eng
    URI
    https://uvadoc.uva.es/handle/10324/64481
    Tipo de versión
    info:eu-repo/semantics/publishedVersion
    Derechos
    openAccess
    Aparece en las colecciones
    • DEP06 - Artículos de revista [352]
    • DEP11 - Artículos de revista [242]
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    Universidad de Valladolid

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