Impaired healing of cutaneous wound in a Trpv1 deficient mouse

Kazuki Ueno1, Shizuya Saika2, Yuka Okada2

  • 1Department of Plastic and Reconstructive Surgery, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan.

Experimental Animals
|November 27, 2022
PubMed

Insights

Transient Receptor Potential vanilloid 1 (TRPV1) loss impairs skin wound healing by prolonging neutrophilic inflammation and Neutrophil Extracellular Traps (NETs) formation. This suggests TRPV1 plays a key role in regulating immune responses during cutaneous repair.

Area of Science:

  • Immunology
  • Dermatology
  • Molecular Biology

Background:

  • Transient Receptor Potential (TRP) ion channels, including TRP vanilloid 1 (TRPV1), are involved in cellular responses to stimuli.
  • TRPV1's role in skin function is known, but its specific involvement in cutaneous wound healing remains unclear.

Purpose of the Study:

  • To investigate the function of TRPV1 in cutaneous wound healing.
  • To elucidate the mechanisms underlying TRPV1's influence on skin repair processes.

Main Methods:

  • Utilized Trpv1-null (KO) and wild-type (WT) C57BL/6 mice to create dorsal circular excisional injuries.
  • Performed macroscopic and histological analyses to assess wound closure, re-epithelialization, and immune cell infiltration.
  • Quantified neutrophil and macrophage populations, as well as Neutrophil Extracellular Traps (NETs) formation.

Main Results:

  • Cutaneous lesions were significantly larger in KO mice compared to WT mice at postoperative days 7 and 10.
  • KO mice exhibited delayed re-epithelialization at postoperative day 7.
  • KO mice showed sustained neutrophil levels and increased NETs formation, unlike WT mice, indicating prolonged neutrophilic inflammation.

Conclusions:

  • Loss of TRPV1 exacerbates cutaneous wound healing defects in mice.
  • TRPV1 appears to regulate neutrophilic inflammation and NETs formation, impacting skin repair.
  • This study highlights a novel link between TRPV1 and the control of neutrophilic responses in wound healing.

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