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The Circular RNA Interacts with STAT3, Increasing Its Nuclear Translocation and Wound Repair by Modulating Dnmt3a and

Zhen-Guo Yang1, Faryal Mehwish Awan2, William W Du3

  • 1Sunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, ON M4N 3M5, Canada; Institute of Animal Nutrition, Sichuan Agricultural University, 211 Huimin Road, Wenjiang District, Chengdu, 611130 Sichuan, China; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5S 1A8, Canada.

Molecular Therapy : the Journal of the American Society of Gene Therapy
|July 6, 2017
PubMed

Insights

Circular RNA circ-Amotl1 significantly accelerates skin wound healing by boosting cell repair mechanisms. This discovery offers potential new treatments for impaired wound healing in conditions like diabetes.

Area of Science:

  • Molecular Biology
  • Regenerative Medicine
  • Biochemistry

Background:

  • Delayed wound healing is a significant global health concern, particularly impacting patients with diabetes and atherosclerosis.
  • Understanding the molecular mechanisms regulating skin repair is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To investigate the role of circular RNA circ-Amotl1 in accelerating the skin wound healing process.
  • To elucidate the molecular pathways through which circ-Amotl1 enhances wound repair.

Main Methods:

  • Utilized a mouse excisional wound model to assess the impact of circ-Amotl1 on healing.
  • Employed molecular biology techniques to analyze protein and microRNA expression levels (Stat3, Dnmt3a, miR-17-5p, fibronectin).
  • Investigated protein-protein interactions and subcellular localization (Stat3, Dnmt3a).

Main Results:

  • Ectopic expression of circ-Amotl1 accelerated wound healing in mice.
  • Circ-Amotl1 increased Stat3 and Dnmt3a protein levels.
  • Dnmt3a methylated miR-17 promoter, decreasing miR-17-5p and increasing fibronectin; Stat3 was also a miR-17-5p target.
  • Circ-Amotl1 promoted Stat3 nuclear translocation and interaction with the Dnmt3a promoter, enhancing its transcription.
  • These molecular changes collectively promoted cell adhesion, migration, proliferation, and survival, leading to improved wound repair.

Conclusions:

  • Circular RNA circ-Amotl1 effectively accelerates skin wound healing.
  • The mechanism involves the circ-Amotl1/Stat3/Dnmt3a/miR-17-5p pathway, enhancing cellular repair processes.
  • Ectopic application of circ-Amotl1 shows promise for clinical applications in treating impaired wound healing.
Keywords:
Dnmt3aStat3circ-Amotl1circRNAcircular RNAwound healing

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