Tafazzin knockdown interrupts cell cycle progression in cultured neonatal ventricular fibroblasts

Quan He, Miao Wang, Nicole Harris, Xianlin Han

Research output: Contribution to journalArticlepeer-review

28 Scopus citations


Mutation of the mitochondrial protein tafazzin causes dilated cardiomyopathy in Barth syndrome. Previous studies have shown that tafazzin knockdown promotes hypertrophy of neonatal cardiac myocytes. The current investigation was designed to show whether tafazzin knockdown affects cardiac fibroblast proliferation and collagen secretion, which contribute to fibrosis in dilated cardiomyopathy. In primary cultures of neonatal ventricular fibroblasts (NVFs) transduced with a tafazzin short hairpin RNA adenovirus, tafazzin knockdown increased production of reactive oxygen species and activation of mitogen-activated protein kinases and induced protein and DNA synthesis via cell cycle regulators. It also reduced intracellular ATP, activated AMPK, and caused multinucleation, hypertrophy, and enhanced collagen secretion. We concluded that tafazzin knockdown interrupts the NVF cell cycle and this in turn may contribute to fibrosis and dilated cardiomyopathy in Barth syndrome.

Original languageEnglish (US)
Pages (from-to)H1332-H1343
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number9
StatePublished - Nov 1 2013
Externally publishedYes


  • Cardiolipin
  • Cell cycle
  • Mitogen-activated protein kinase
  • Reactive oxygen species

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)
  • Physiology


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