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PPP1R12C Promotes Atrial Hypocontractility in Atrial Fibrillation.

Srikanth Perike1,2,3, Francisco J Gonzalez-Gonzalez1,2,3, Issam Abu-Taha4

  • 1Division of Cardiology, Department of Medicine, College of Medicine (S.P., F.J.G.-G., K.S.L., A.A., A.E.C., A.S., J.G., S.-G.O., D. Darbar, B.M.W., M.D.M.), University of Illinois at Chicago.

Circulation Research
|September 22, 2023
PubMed
Summary

Increased PPP1R12C protein in atrial fibrillation (AF) reduces atrial contractility by dephosphorylating MLC2a. This molecular mechanism contributes to stroke risk in AF patients.

Keywords:
arrhythmias, cardiacatrial fibrillationmyosin light chainsprotein phosphatase 1stroke volume

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Atrial fibrillation (AF) is the most common cardiac arrhythmia, significantly increasing stroke risk.
  • Atrial hypocontractility is a known contributor to stroke risk in AF, but its molecular basis is unclear.
  • This study investigates the role of PPP1R12C (protein phosphatase 1 regulatory subunit 12C) in AF-related atrial hypocontractility.

Purpose of the Study:

  • To test the hypothesis that increased PPP1R12C expression causes atrial hypocontractility by reducing MLC2a (atrial myosin light chain 2) phosphorylation.
  • To elucidate the molecular mechanisms linking PPP1R12C, PP1 (protein phosphatase 1), and MLC2a in AF.

Main Methods:

  • Analysis of human atrial appendage tissues from AF patients and controls.
  • Western blotting, coimmunoprecipitation, and phosphorylation studies to assess protein interactions and modifications.
  • In vitro studies using HL-1 cells and pharmacological inhibitors, and in vivo studies with cardiac-specific lentiviral PPP1R12C overexpression in mice.

Main Results:

  • Human AF patients showed a 2-fold increase in PPP1R12C expression and a >40% reduction in MLC2a phosphorylation compared to controls.
  • Increased PPP1R12C-PP1c and PPP1R12C-MLC2a binding was observed in AF.
  • Mice with PPP1R12C overexpression exhibited enlarged atria, reduced atrial function, and significantly higher AF inducibility.

Conclusions:

  • Elevated PPP1R12C levels in AF patients correlate with reduced atrial contractility.
  • PPP1R12C overexpression in mice leads to MLC2a dephosphorylation, decreased atrial contractility, and increased AF susceptibility.
  • PP1 regulation of sarcomere function via MLC2a is a critical factor in atrial contractility during AF.