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A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
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A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

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EphB2 signaling-mediated Sirt3 expression reduces MSC senescence by maintaining mitochondrial ROS homeostasis

Young Hyun Jung1, Hyun Jik Lee1, Jun Sung Kim1

  • 1Department of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research Center, Seoul National University, Seoul 08826, Republic of Korea.

Free Radical Biology & Medicine
|July 9, 2017
PubMed

Insights

Activating EphB2 signaling in umbilical cord-derived mesenchymal stem cells (UCB-MSCs) reduces mitochondrial reactive oxygen species (mtROS) and enhances wound healing. This occurs via Nrf-2-dependent Sirt3 expression, boosting MnSOD activity.

Area of Science:

  • Stem Cell Biology
  • Mitochondrial Biology
  • Wound Healing Research

Background:

  • Mitochondrial reactive oxygen species (mtROS) homeostasis disruption drives UCB-MSC senescence.
  • Preventing mtROS accumulation is crucial for suppressing UCB-MSC senescence.

Purpose of the Study:

  • To investigate the role of EphB2 signaling in UCB-MSC senescence and therapeutic potential.
  • To elucidate the molecular mechanisms linking EphB2, Sirt3, and mtROS regulation.

Main Methods:

  • Studied EphrinB2/EphB2 expression in UCB-MSCs during passaging.
  • Investigated EphB2-induced Sirt3 mitochondrial translocation and Nrf-2 nuclear translocation.
  • Assessed MnSOD activity and mtROS levels following EphB2 activation.
  • Evaluated the therapeutic effect of UCB-MSCs in skin-wound healing models.

Main Results:

  • EphB2 signaling induced Sirt3 mitochondrial translocation, dependent on SIRT3.
  • EphrinB2-Fc treatment promoted Nrf-2 nuclear translocation via c-Src phosphorylation, regulating Sirt3.
  • EphB2 signaling increased MnSOD and reduced mtROS by Sirt3-mediated deacetylation of MnSOD.
  • EphB2 activation enhanced UCB-MSC therapeutic efficacy in skin-wound healing.

Conclusions:

  • EphB2 activation optimizes UCB-MSC therapeutic use in wound repair.
  • The mechanism involves MnSOD-mediated mtROS scavenging via the EphB2/c-Src/Nrf-2/Sirt3 pathway.
  • EphB2 represents a novel therapeutic target for enhancing UCB-MSC functions.
Keywords:
AgingEphrinEphrin receptorMesenchymal stem cellMitochondrial ROSMnSODSirtuin

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