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Transient Receptor Potential Channel Canonical Type 3 Deficiency Antagonizes Myofibroblast Transdifferentiation In

Weijie Xia1, Qianran Wang2, Yuangang Lu3

  • 1Department of Burn & Plastic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Biomed Research International
|March 29, 2020
PubMed
Abstract

Insights

Transforming growth factor-beta 1 (TGFβ1) activates transient receptor potential channel canonical type 3 (TRPC3), increasing reactive oxygen species (ROS) and promoting myofibroblast transdifferentiation. Inhibiting TRPC3 may limit scar tissue formation after injury.

Area of Science:

  • Cell Biology
  • Physiology
  • Biochemistry

Background:

  • Myofibroblast differentiation is linked to reactive oxygen species (ROS) production by NADPH oxidase (Nox4).
  • Transient receptor potential channel canonical type 3 (TRPC3) inhibition affects mitochondrial calcium handling and ROS in hypertension.
  • The role of TRPC3 in regulating mitochondrial calcium, ROS, and myofibroblast transdifferentiation during wound healing is unclear.

Purpose of the Study:

  • To investigate whether TRPC3 regulates mitochondrial calcium and ROS production.
  • To determine TRPC3's role in myofibroblast transdifferentiation during wound healing.

Main Methods:

  • Utilized transforming growth factor-beta 1 (TGFβ1) to activate TRPC3 in cell cultures.
  • Administered TRPC3 inhibitor (Pyr3) to assess its effects on TGFβ1-induced responses.
  • Examined myofibroblast transdifferentiation markers like alpha-smooth muscle actin (αSMA).
  • Studied TRPC3 knockout (Trpc3-/-) mice to evaluate in vivo effects.

Main Results:

  • TGFβ1 activated TRPC3, leading to increased mitochondrial calcium and ROS production.
  • Pyr3 significantly reduced TGFβ1-induced αSMA expression and myofibroblast differentiation.
  • Trpc3-/- mice showed significantly reduced myofibroblast transdifferentiation.

Conclusions:

  • TGFβ1-mediated TRPC3 activation enhances mitochondrial calcium and ROS production, promoting myofibroblast transdifferentiation and hypertrophic scar (HTS) formation.
  • Targeting the TRPC3-Nox4/pSmad2/3 pathway could be a therapeutic strategy to reduce HTS formation post-injury.

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