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Nitric oxide induces epidermal stem cell de-adhesion by targeting integrin β1 and Talin via the cGMP signalling

Rixing Zhan1, Fan Wang2, Ying Wu3

  • 1Institute of Burn Research, State Key Laboratory of Trauma, Burn and Combined Injury, Key Laboratory of Proteomics of Chongqing, Southwest Hospital, The Third Military Medical University (Army Medical University), Chongqing 400038, China; School of Nursing, The Third Military Medical University (Army Medical University), Chongqing 400038, China.

Nitric Oxide : Biology and Chemistry
|April 27, 2018
PubMed
Abstract

Insights

Nitric oxide (NO) promotes epidermal stem cell (ESC) de-adhesion and wound healing by regulating integrin β1 and Talin phosphorylation via the cGMP pathway. This study elucidates NO

Area of Science:

  • Cell Biology
  • Wound Healing Research
  • Biochemistry

Background:

  • Nitric oxide (NO) is crucial for wound healing, but its precise mechanisms remain unclear.
  • Understanding NO's role in epidermal stem cell (ESC) behavior is key to advancing wound repair therapies.

Purpose of the Study:

  • To investigate the effect of NO on ESC de-adhesion.
  • To elucidate the underlying molecular mechanisms, including integrin β1 and Talin phosphorylation.
  • To confirm NO's role in wound healing in vivo.

Main Methods:

  • Assessed ESC de-adhesion using NO donor S-nitroso-N-acetyl penicillamine (SNAP) and integrin β1/collagen IV assays.
  • Analyzed integrin β1 expression and Talin phosphorylation via Western blot and real-time PCR.
  • Utilized sGC and PKG inhibitors/agonists to explore signaling pathways.
  • Validated findings in vivo using scald and excision wound models.

Main Results:

  • SNAP enhanced ESC de-adhesion in a dose-dependent manner.
  • Integrin β1 expression and Talin phosphorylation were inversely correlated with SNAP concentration.
  • Inhibitors of soluble guanylyl cyclase (sGC) and protein kinase G (PKG) blocked NO's effects.
  • NO's role in wound healing via integrin β1 and cGMP signaling was confirmed in vivo.

Conclusions:

  • NO stimulates ESC de-adhesion by modulating integrin β1 expression and Talin phosphorylation.
  • The cGMP signaling pathway mediates NO's effects on ESCs and is implicated in wound healing.
Keywords:
Cell de-adhesionEpidermal stem cellsIntegrin β1Nitric oxide

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