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Murine Dermal Fibroblast Isolation by FACS
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Selective deletion of PPARβ/δ in fibroblasts causes dermal fibrosis by attenuated LRG1 expression

Ming Keat Sng1,2, Jeremy Soon Kiat Chan1, Ziqiang Teo1

  • 11School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore, 637551 Singapore.

Cell Discovery
|April 6, 2018
PubMed

Insights

This study reveals how fibroblast PPARβ/δ regulates LRG1, a key gene in skin health and dermal fibrosis. This finding offers new insights into connective tissue diseases and potential therapeutic targets.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Genetics

Background:

  • Connective tissue diseases involve excessive collagen deposition, impacting skin and organs.
  • Fibroblasts are crucial in the pathology of these conditions.
  • Peroxisome-proliferator activated receptors (PPARs) are therapeutic targets for dermal fibrosis, but subtype roles are unclear.

Purpose of the Study:

  • To investigate the role of fibroblast PPARβ/δ in dermal fibrosis.
  • To identify novel genes regulated by fibroblast PPARβ/δ in skin.

Main Methods:

  • Generated a fibroblast-specific PPARβ/δ knockout mouse model (FSPCre-Pparb/d-/-).
  • Analyzed epidermal and dermal transcriptome profiles of the knockout mice.

Main Results:

  • Discovered downregulated leucine-rich alpha-2-glycoprotein-1 (LRG1) in knockout mice.
  • Identified LRG1 as a novel gene in skin development and architecture.
  • Demonstrated that fibroblast PPARβ/δ regulates LRG1, integrating PPARβ/δ and TGFβ1 signaling.

Conclusions:

  • Fibroblast PPARβ/δ plays a significant role in skin homeostasis and dermal fibrosis.
  • LRG1 is a novel downstream target of PPARβ/δ in fibroblasts.
  • The FSPCre-Pparb/d-/- mouse model is a valuable tool for studying dermal fibrosis.

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