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RNA-Binding Protein LIN28a Regulates New Myocyte Formation in the Heart Through Long Noncoding RNA-H19.

Vagner Oliveira Carvalho Rigaud1, Robert C Hoy1, Justin Kurian1

  • 1Center for Metabolic Disease Research (V.0.C.R., R.C.H., J.K., C.Z., M.B., I.B., J.P., T.P., M.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA.

Circulation
|October 31, 2022
PubMed
Summary

RNA-binding protein LIN28a reprograms metabolism in mononuclear diploid cardiomyocytes, promoting their persistence and enhancing cardiac repair after injury. This discovery links cardiomyocyte metabolism to ploidy regulation and heart regeneration.

Keywords:
RNA-binding proteinsmetabolismmyocytes, cardiacploidiesregeneration

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Area of Science:

  • Cardiovascular Biology
  • Regenerative Medicine
  • Molecular Metabolism

Background:

  • The mature heart has limited regenerative capacity due to cardiomyocyte cell cycle exit and polyploidization.
  • Cardiomyocyte metabolism shifts postnatally, coinciding with the loss of regenerative potential.
  • The role of metabolic reprogramming in maintaining regenerative cardiomyocyte populations is unknown.

Purpose of the Study:

  • To investigate the role of RNA-binding protein LIN28a in cardiac repair.
  • To determine if LIN28a can maintain regenerative mononuclear diploid cardiomyocytes.
  • To link metabolic reprogramming to cardiomyocyte ploidy and cardiac regeneration.

Main Methods:

  • LIN28a overexpression in mouse models (transgenesis, neonatal/adult cell culture, myocardial injury models).
  • Assessment of cardiomyocyte number, cell cycle status, and ploidy.
  • Metabolic analysis (glycolysis, ATP production, enzyme levels) in LIN28a-overexpressing cardiomyocytes.
  • RNA-immunoprecipitation sequencing to identify LIN28a targets.

Main Results:

  • LIN28a overexpression in postnatal hearts reduced polyploidization and increased cardiomyocyte cell cycle activity.
  • LIN28a enhanced cardiac function and survival after injury in both young and adult mice.
  • LIN28a increased glycolysis and ATP production in cardiomyocytes, with long noncoding RNA-H19 identified as a key target.
  • Inhibition of LIN28a or H19 blunted these pro-reparative effects.

Conclusions:

  • LIN28a reprograms cardiomyocyte metabolism, promoting the persistence of mononuclear diploid cells.
  • This metabolic reprogramming enhances cardiac repair and function after injury.
  • LIN28a links cardiomyocyte metabolism to the regulation of ploidy and cardiac regenerative processes.