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Carvedilol Suppresses Apoptosis and Ion Channel Remodelling of HL-1 Cardiac Myocytes Expressing E334K cMyBPC.
Endo, R; Bahrudin, U; Notsu, T; Tanno, S; Onohara, T; Yamaguchi, S; Ikeda, N; Surastri, B; Nakayama, Y; Ninomiya, H; Shirayoshi, Y; Inagaki, Y; Yamamoto, K; Yoshida, A; Hisatome, I.
Afiliação
  • Endo R; Department of Anesthesiology, Tottori University Faculty of Medicine, Yonago, Japan.
  • Bahrudin U; Division of Regenerative Medicine and Therapeutics, Tottori University Graduate School of Medical Science, Yonago, Japan.
  • Notsu T; Division of Regenerative Medicine and Therapeutics, Tottori University Graduate School of Medical Science, Yonago, Japan.
  • Tanno S; Division of Regenerative Medicine and Therapeutics, Tottori University Graduate School of Medical Science, Yonago, Japan.
  • Onohara T; Division of Organ Regeneration Surgery, Tottori University Faculty of Medicine, Yonago, Japan.
  • Yamaguchi S; Division of Regenerative Medicine and Therapeutics, Tottori University Graduate School of Medical Science, Yonago, Japan.
  • Ikeda N; Division of Regenerative Medicine and Therapeutics, Tottori University Graduate School of Medical Science, Yonago, Japan.
  • Surastri B; Department of Pharmacology, Diponegoro University Faculty of Medicine, Semarang, Indonesia.
  • Nakayama Y; Division of Functional Genomics, Research Center for Bioscience and Technology, Tottori University, Yonago, Japan.
  • Ninomiya H; Department of Biological Regulation, Tottori University Faculty of Medicine, Yonago, Japan.
  • Shirayoshi Y; Division of Regenerative Medicine and Therapeutics, Tottori University Graduate School of Medical Science, Yonago, Japan.
  • Inagaki Y; Department of Anesthesiology, Tottori University Faculty of Medicine, Yonago, Japan.
  • Yamamoto K; Department of Multidisciplinary Internal Medicine, School of Medicine, Tottori University, Yonago, Japan.
  • Yoshida A; Division of Regenerative Medicine and Therapeutics, Tottori University Graduate School of Medical Science, Yonago, Japan.
  • Hisatome I; Division of Regenerative Medicine and Therapeutics, Tottori University Graduate School of Medical Science, Yonago, Japan.
Drug Res (Stuttg) ; 66(3): 126-9, 2016 Mar.
Article em En | MEDLINE | ID: mdl-26479129
ABSTRACT

BACKGROUND:

Besides its antiarrhythmic action, carvedilol has an activity to suppress cardiac tissue damage. However, it is unknown whether it has any effect on cellular apoptosis and ion channel remodelling.

PURPOSE:

To know whether carvedilol has any effect on apoptosis and ion channel remodeling of HL-1 cells expressing E334K MyBPC, and comparing it with bisoprolol.

METHOD:

We examined effects of carvedilol and bisoprolol on the levels of pro- and anti-apoptotic proteins and ion channels as well as apoptosis of HL-1 cells transfected with E334K MyBPC using Western blot and flow cytometry.

RESULTS:

Carvedilol decreased the protein levels of p53, Bax and cytochrome c and increased that of Bcl-2 in HL-1 cells expressing E334K MyBPC. Bisoprolol failed to affect the protein levels. Both carvedilol and bisoprolol increased the protein levels of Cav1.2 but not that of Nav1.5. Carvedilol was stronger than bisoprolol at decreasing the number of annexin-V positive cells in HL-1 cells expressing E334K MyBPC.

CONCLUSION:

Carvedilol suppressed apoptosis of HL-1 cells expressing E334K MyBPC through modification of pro- and anti-apoptotic proteins, whose was associated with an increase of Cav 1.2 protein expression.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Propanolaminas / Carbazóis / Proteínas de Transporte / Apoptose / Miócitos Cardíacos / Canais Iônicos Limite: Humans Idioma: En Revista: Drug Res (Stuttg) Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Japão

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Propanolaminas / Carbazóis / Proteínas de Transporte / Apoptose / Miócitos Cardíacos / Canais Iônicos Limite: Humans Idioma: En Revista: Drug Res (Stuttg) Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Japão