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Regulation of cardiac excitation-contraction coupling by sorcin, a novel modulator of ryanodine receptors
Farrell, Emily F; Antaramian, Anaid; Benkusky, Nancy; Zhu, Xinsheng; Rueda, Angélica; Gómez, Ana M; Valdivia, Héctor H.
Afiliação
  • Farrell, Emily F; University of Wisconsin Medical School. Department of Physiology. US
  • Antaramian, Anaid; University of Wisconsin Medical School. Department of Physiology. US
  • Benkusky, Nancy; University of Wisconsin Medical School. Department of Physiology. US
  • Zhu, Xinsheng; University of Wisconsin Medical School. Department of Physiology. US
  • Rueda, Angélica; University of Wisconsin Medical School. Department of Physiology. US
  • Gómez, Ana M; INSERM. Montepellier. FR
  • Valdivia, Héctor H; University of Wisconsin Medical School. Department of Physiology. US
Biol. Res ; 37(4): 609-612, 2004. ilus
Article em En | LILACS | ID: lil-437515
Biblioteca responsável: CL1.1
ABSTRACT
Activation of Ca2+ release channels/ryanodine receptors (RyR) by the inward Ca2+ current (ICa) gives rise to Ca2+-induced Ca2+ release (CICR), the amplifying Ca2+ signaling mechanism that triggers contraction of the heart. CICR, in theory, is a high-gain, self-regenerating process, but an unidentified mechanism stabilizes it in vivo. Sorcin, a 21.6 kDa Ca2+-binding protein, binds to cardiac RyRs with high affinity and completely inhibits channel activity. Sorcin significantly inhibits both the spontaneous activity of RyRs in quiescent cells (visualized as Ca2+ sparks) and the ICa-triggered activity of RyRs that gives rise to [Ca2+]i transients. Since sorcin decreases the amplitude of the [Ca2+]i transient without affecting the amplitude of ICa, the overall effect of sorcin is to reduce the "gain" of excitation-contraction coupling. Immunocytochemical staining shows that sorcin localizes to the dyadic space of ventricular cardiac myocytes. Ca2+ induces conformational changes and promotes translocation of sorcin between soluble and membranous compartments, but the [Ca2+] required for the latter process (ED50 = ~200 mM) appears to be reached only within the dyadic space. Thus, sorcin is a potent inhibitor of both spontaneous and ICa-triggered RyR activity and may play a role in helping terminate the positive feedback loop of CICR.
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Texto completo: 1 Coleções: 01-internacional Base de dados: LILACS Assunto principal: Retículo Sarcoplasmático / Proteínas de Ligação ao Cálcio / Canal de Liberação de Cálcio do Receptor de Rianodina / Miócitos Cardíacos / Contração Miocárdica Limite: Animals Idioma: En Revista: Biol. Res Assunto da revista: BIOLOGIA Ano de publicação: 2004 Tipo de documento: Article País de afiliação: França / Estados Unidos País de publicação: Chile
Texto completo
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Texto completo: 1 Coleções: 01-internacional Base de dados: LILACS Assunto principal: Retículo Sarcoplasmático / Proteínas de Ligação ao Cálcio / Canal de Liberação de Cálcio do Receptor de Rianodina / Miócitos Cardíacos / Contração Miocárdica Limite: Animals Idioma: En Revista: Biol. Res Assunto da revista: BIOLOGIA Ano de publicação: 2004 Tipo de documento: Article País de afiliação: França / Estados Unidos País de publicação: Chile