Related Experiment Video

Updated: Jan 15, 2026

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
04:41

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue

Published on: July 28, 2023

3.3K

Mesenchymal stem cells attenuate keloid pathogenesis via TGF-β1/SMAD-driven MMP9 suppression: mechanistic insights

Yujia Zhao1, Hexiao Zhang2,3, Qiuyan Han1

  • 1Department of Plastic and Medical Aesthetic Surgery, The Second Hospital of Tianjin Medical University, No. 23 Pingjiang Road, Hexi District, Tianjin 300211, China.

Blood Science (Baltimore, Md.)
|October 16, 2025
PubMed

Insights

Mesenchymal stem cells (MSCs) reduce keloid fibroblast activity by suppressing matrix metalloproteinases 9 (MMP9) via the transforming growth factor-β1/SMAD pathway. This study reveals MSCs

Area of Science:

  • Cell biology
  • Dermatology
  • Regenerative Medicine

Background:

  • Keloids present therapeutic challenges due to excessive collagen and recurrence.
  • Mesenchymal stem cells (MSCs) show promise for keloid treatment, but mechanisms are unclear.
  • Understanding MSCs' role in extracellular matrix (ECM) remodeling is crucial for keloid pathogenesis.

Purpose of the Study:

  • To investigate how MSCs modulate ECM remodeling in keloid pathogenesis.
  • To elucidate the specific molecular mechanisms by which MSCs affect keloid fibroblasts.
  • To identify potential therapeutic targets for keloid treatment.

Main Methods:

  • Co-culture of human umbilical cord MSCs (UC-MSCs) with immortalized keloid fibroblasts (HDIKFs).
  • Assays used: CCK8 for proliferation, wound healing for migration, quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) for gene expression.
  • Analysis of key signaling pathways: transforming growth factor-β1/SMAD (TGF-β1/SMAD), hypoxia-inducible factor-1α (HIF-1α), and interleukin-10 receptor alpha (IL-10RA).

Main Results:

  • UC-MSCs significantly suppressed keloid fibroblast proliferation and migration in vitro.
  • UC-MSCs selectively downregulated matrix metalloproteinases 9 (MMP9) expression in keloid fibroblasts.
  • Suppression of MMP9 was linked to inhibition of the TGF-β1/SMAD pathway, reduced HIF-1α and SMAD2, and increased IL-10RA.

Conclusions:

  • MSCs attenuate keloid fibroblast activity via TGF-β1/SMAD-driven MMP9 suppression and IL-10RA enhancement.
  • MMP9 is identified as a key therapeutic target for keloid management.
  • Findings provide a foundation for optimizing MSC-based therapies for ECM homeostasis in keloids.
Keywords:
HDIKFsKeloidMMP9TGF-β1/SMADUC-MSCs

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