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Rictor/mTORC2 involves mitochondrial function in ES cells derived cardiomyocytes via mitochondrial Connexin 43.

Jia-Dan Wang1,2, Ying Shao1, Dan Liu1

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Acta Pharmacologica Sinica
|February 6, 2021
PubMed
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Knockdown of Rictor impairs cardiomyocyte function by disrupting mitochondrial connexin 43 (Cx43) transport. This leads to mitochondrial damage and impaired cellular energy production in stem cell-derived cardiomyocytes.

Keywords:
Connexin43Rictor/mTORC2cardiomyocyte differentiationembryonic stem cellmitochondria

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Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Biology
  • Stem Cell Differentiation

Background:

  • Rictor is essential for mTORC2 signaling and Akt phosphorylation.
  • Rictor knockdown impairs cardiomyocyte differentiation and electrophysiology.
  • Rictor knockdown reduces connexin 43 (Cx43) expression, affecting mitochondrial Cx43 (mtCx43).

Purpose of the Study:

  • To investigate the mechanisms of mitochondrial damage in Rictor-knockdown cardiomyocytes.
  • To elucidate the role of mtCx43 in Rictor-mediated mitochondrial dysfunction.

Main Methods:

  • Utilized mouse embryonic stem (ES) cell differentiation model.
  • Performed transmission electron microscopy to assess mitochondrial morphology.
  • Measured ATP production, mitochondrial membrane potential, and respiratory chain complex activity.
  • Investigated Cx43 translocation, mTOR/Akt signaling, HDAC6 expression, and Hsp90 acetylation.

Main Results:

  • Rictor knockdown caused mitochondrial swelling and rupture.
  • Decreased ATP production, mitochondrial transmembrane potential, and respiratory chain activity were observed.
  • Cx43 translocation into mitochondria was inhibited.
  • mTOR/Akt pathway inactivation led to reduced HDAC6, increased Hsp90 acetylation, and impaired Hsp90-Cx43-TOM20 complex formation.

Conclusions:

  • Mitochondrial Cx43 is crucial in Rictor knockdown-induced mitochondrial damage.
  • Rictor regulates mitochondrial function via the mTOR/Akt/HDAC6/Hsp90 pathway affecting mtCx43.
  • Targeting Rictor or its downstream effectors may offer therapeutic strategies for cardiac mitochondrial dysfunction.