AI Article Synopsis

  • TRPV4 is a cation ion channel found in various cells and has been observed to play a role in wound healing, particularly in the skin.
  • In experiments with mice, TRPV4 knockout (KO) mice showed impaired wound healing compared to wild-type (WT) mice, including delays in re-epithelialization and collagen formation.
  • The study concluded that TRPV4 is crucial for the migration and differentiation of skin cells, promoting better wound healing through increased collagen deposition.

Article Abstract

Background: Transient receptor potential vanilloid 4 (TRPV4), a cation ion channel, is expressed in different cells, and it regulates the development of different diseases. We recently found a high TRPV4 expression in the wounded skin area. However, the role of TRPV4 in cutaneous wound healing is unknown.

Objective: To investigate the role of TRPV4 in cutaneous wound healing in a mouse model.

Methods: Skin wound healing experiment and histopathological studies were performed between WT and TRPV4 KO mice. The effect of TRPV4 antagonist and agonist on cell migration, proliferation, and differentiation were examined in vitro.

Results: TRPV4 expression was enhanced in wounded area in the skin. TRPV4 KO mice had impaired cutaneous wound healing compared with the WT mice. Further, they had significantly suppressed re-epithelialization and formation of granulation tissue, amount of collagen deposition, and number of α-SMA-positive myofibroblasts in skin wounds. qPCR revealed that the KO mice had decreased mRNA expression of COL1A1 and ACTA2 in skin wounds. In vitro, treatment with selective TRPV4 antagonist suppressed migrating capacity, scratch stimulation enhanced the expression of phospho-ERK in keratinocytes, and TGF-β stimulation enhanced the mRNA expression of COL1A1 and ACTA2 in fibroblasts. Selective TRPV4 agonist suppressed cell migration in keratinocytes, and did not enhance proliferation and migration, but promoted differentiation in fibroblasts.

Conclusion: TRPV4 mediates keratinocytes and fibroblasts migration and increases collagen deposition in the wound area, thereby promoting cutaneous wound healing.

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Source
http://dx.doi.org/10.1016/j.jdermsci.2023.10.002DOI Listing

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