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CCN6 regulates mitochondrial function.

Milan Patra1, Sushil K Mahata2, Deepesh K Padhan1

  • 1Cancer Biology and Inflammatory Disorder Division, CSIR-Indian institute of Chemical Biology, 4-Raja S.C. Mullick Road, Jadavpur, Kolkata 700032, India.

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|June 3, 2016
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Summary
This summary is machine-generated.

CCN6 protein regulates mitochondrial function and reactive oxygen species (ROS) levels. Nrf2 transcription factor balances CCN6 expression, impacting cellular respiration and mitochondrial health.

Keywords:
CCN6MitochondriaNrf2PGC1α

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Area of Science:

  • Cell Biology
  • Mitochondrial Biology
  • Biochemistry

Background:

  • CCN6 (WISP3) is linked to progressive pseudo rheumatoid dysplasia, but its precise function is unclear.
  • A negative correlation exists between CCN6 expression and reactive oxygen species (ROS) accumulation.
  • Mitochondrial dysfunction is implicated in various pathologies.

Purpose of the Study:

  • To investigate the role of CCN6 in regulating mitochondrial function and ROS production.
  • To determine if CCN6 influences mitochondrial respiration and ATP synthesis.
  • To explore the relationship between CCN6, Nrf2, and mitochondrial biogenesis.

Main Methods:

  • Depletion of CCN6 in chondrocyte cell line C-28/I2 using siRNA.
  • Analysis of mitochondrial electron transport chain (ETC) activity, respiration, and ROS levels.
  • Measurement of mitochondrial membrane potential, ATP synthesis, and Ca(2+) flux.
  • Assessment of PGC1α induction, mitochondrial mass, and morphology.
  • Investigation of Nrf2's effect on CCN6 expression.

Main Results:

  • CCN6 was found to localize in mitochondria.
  • CCN6 depletion led to altered mitochondrial respiration and increased ROS levels.
  • Enhanced ETC activity correlated with increased mitochondrial ATP synthesis and membrane potential.
  • CCN6-depleted cells showed ROS-dependent PGC1α induction, increased mitochondrial mass, and altered morphology.
  • Nrf2 was identified as a repressor of CCN6 expression.

Conclusions:

  • CCN6 functions as a molecular brake in regulating mitochondrial function.
  • Nrf2 plays a role in balancing CCN6 expression and mitochondrial homeostasis.
  • These findings provide new insights into CCN6's role beyond its association with skeletal dysplasia, highlighting its impact on mitochondrial dynamics and cellular redox balance.