Prestin amplifies cardiac motor functions

Xiaodong Zhang, Phung N. Thai, Lu Ren, Maria Cristina Perez Flores, Hannah A. Ledford, Seojin Park, Jeong Han Lee, Choong Ryoul Sihn, Che Wei Chang, Wei Chun Chen, Valeriy Timofeyev, Jian Zuo, James W. Chan, Ebenezer N Yamoah, Nipavan Chiamvimonvat

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

Cardiac cells generate and amplify force in the context of cardiac load, yet the membranous sheath enclosing the muscle fibers—the sarcolemma—does not experience displacement. That the sarcolemma sustains beat-to-beat pressure changes without experiencing significant distortion is a muscle-contraction paradox. Here, we report that an elastic element—the motor protein prestin (Slc26a5)—serves to amplify actin-myosin force generation in mouse and human cardiac myocytes, accounting partly for the nonlinear capacitance of cardiomyocytes. The functional significance of prestin is underpinned by significant alterations of cardiac contractility in Prestin-knockout mice. Prestin was previously considered exclusive to the inner ear's outer hair cells; however, our results show that prestin serves a broader cellular motor function.

Original languageEnglish (US)
Article number109097
JournalCell Reports
Volume35
Issue number5
DOIs
StatePublished - May 4 2021

Keywords

  • actin-myosin force generation
  • cardiac contraction
  • cardiomyocytes
  • human ventricular myocytes
  • nonlinear capacitance
  • outer hair cells
  • prestin
  • Slc26a5
  • solute carrier gene family
  • systolic and diastolic dysfunction

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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