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Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor
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RNase-induced apoptosis: fate of calcium-activated potassium channels

Olga N Ilinskaya1, Andreas Koschinski, Holger Repp

  • 1Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Vavilov str. 32, Moscow 119991, Russia. olga.ilinskaya@ksu.ru

Biochimie
|February 23, 2008
PubMed

Insights

Microbial RNases protect kidney cells from apoptosis by modulating calcium-activated potassium (KCa) channels. RNase activity on KCa channels suggests potential for new anticancer therapies targeting these channels.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Background:

  • Microbial RNases are enzymes that degrade RNA.
  • Calcium-activated potassium (KCa) channels play crucial roles in cellular functions, including apoptosis regulation.
  • The interplay between microbial RNases and KCa channels in cellular protection is not well understood.

Purpose of the Study:

  • To investigate the functional connection between microbial RNases and KCa channels in human kidney cells.
  • To determine the effect of specific microbial RNases (binase and RNase Sa mutant) on KCa channel activity and cell survival.
  • To explore the potential of microbial RNases as therapeutic agents targeting KCa channels for cancer treatment.

Main Methods:

  • Utilized human embryo kidney cells (HEKhSK4) engineered to express KCa channels.
  • Performed whole-cell patch-clamp recordings to measure membrane currents through KCa channels.
  • Assessed cell viability and apoptosis induction by microbial RNases.
  • Monitored intracellular calcium concentration and mitochondrial membrane potential.

Main Results:

  • KCa channels conferred protection to HEKhSK4 cells against RNase-induced apoptosis.
  • RNase treatment induced a biphasic response in KCa channel activity: an initial increase followed by a decrease.
  • Intracellular calcium levels and mitochondrial potential showed dynamic changes over 72 hours post-treatment.
  • KCa channel activity could be restored upon removal of RNases, suggesting a reversible regulatory mechanism.

Conclusions:

  • Microbial RNases modulate KCa channel activity, potentially through transcriptional or translational downregulation.
  • The observed effects suggest a novel mechanism where RNases interact with KCa channels to influence cell fate.
  • These findings highlight the potential of microbial RNases as a basis for developing novel anticancer agents targeting KCa channels.

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