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RBFOX1 Regulates Calcium Signaling and Enhances SERCA2 Translation.

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RBFOX1 protein is crucial for maintaining heart function by regulating calcium handling. Its absence leads to worsened cardiac function and heart failure, particularly under stress.

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Gene Regulation

Background:

  • RBFOX1 (RNA-binding protein, fox-1 homolog 1) is vital for RNA processing in multiple tissues.
  • Its role in cardiac calcium homeostasis and function requires further elucidation.

Purpose of the Study:

  • To investigate the function of RBFOX1 in regulating calcium handling and cardiac performance.
  • To determine the molecular mechanisms by which RBFOX1 influences cardiac function.

Main Methods:

  • Generation of cardiomyocyte-specific Rbfox1 gene-deletion mice (cKO).
  • Assessment of cardiac function, hypertrophy, and heart failure under homeostatic and pressure overload conditions (trans-aortic constriction).
  • Analysis of calcium-handling proteins, calcium dynamics, mRNA expression, RNA immunoprecipitation (RIP), luciferase assays, and puromycin incorporation assays.

Main Results:

  • cKO mice exhibited depressed cardiac function and exacerbated cardiac hypertrophy and heart failure following pressure overload.
  • RBFOX1 deletion led to altered phosphorylation of PLN and CAMKII, decreased SERCA2 expression, and delayed calcium reuptake.
  • RBFOX1 directly binds to Serca2 mRNA and enhances SERCA2 protein translation, indicating post-transcriptional regulation.

Conclusions:

  • RBFOX1 is essential for maintaining cardiac function by regulating calcium homeostasis.
  • RBFOX1 plays a critical post-transcriptional role in controlling SERCA2 expression, impacting cardiac performance.
  • Targeting RBFOX1 may offer therapeutic strategies for heart failure.